To address the issues of reduced performance and shortened lifespan during the low-carbonizating process of Al_(2)O_(3)-C refractories,nano-crystalline ZrC modified graphite was prepared using Zr powder and flake grap...To address the issues of reduced performance and shortened lifespan during the low-carbonizating process of Al_(2)O_(3)-C refractories,nano-crystalline ZrC modified graphite was prepared using Zr powder and flake graphite as raw materials,with NaCl and NaF mixed salt serving as the medium.The flake graphite was gradually replaced by ZrC modified graphite in the preparation of Al_(2)O_(3)-C refractories,and its impact on the material’s structure and properties was investigated.The results indicate that,compared to samples with only flake graphite,the introduction of 1 mass%to 5 mass%nano-crystalline ZrC modified graphite can significantly enhance the mechanical performance of low-carbon Al_(2)O_(3)-C refractories.When 5 mass%ZrC modified graphite is added,the mechanical properties of the samples are optimal,with the cold modulus of rupture and elastic modulus reaching 22.5 MPa and 65.0 GPa,respectively.展开更多
We previously reported that postsynaptic density-93 mediates neuron-microglia crosstalk by interacting with amino acids 357–395 of C-X3-C motif chemokine ligand 1(CX3 CL1) to induce microglia polarization. More impor...We previously reported that postsynaptic density-93 mediates neuron-microglia crosstalk by interacting with amino acids 357–395 of C-X3-C motif chemokine ligand 1(CX3 CL1) to induce microglia polarization. More importantly, the peptide Tat-CX3 CL1(comprising amino acids 357–395 of CX3 CL1) disrupts the interaction between postsynaptic density-93 and CX3 CL1, reducing neurological impairment and exerting a protective effect in the context of acute ischemic stroke. However, the mechanism underlying these effects remains unclear. In the current study, we found that the pro-inflammatory M1 phenotype increased and the anti-inflammatory M2 phenotype decreased at different time points. The M1 phenotype increased at 6 hours after stroke and peaked at 24 hours after perfusion, whereas the M2 phenotype decreased at 6 and 24 hours following reperfusion. We found that the peptide Tat-CX3 CL1(357–395 aa) facilitates microglial polarization from M1 to M2 by reducing the production of soluble CX3 CL1. Furthermore, the a disintegrin and metalloprotease domain 17(ADAM17) inhibitor GW280264 x, which inhibits metalloprotease activity and prevents CX3 CL1 from being sheared into its soluble form, facilitated microglial polarization from M1 to M2 by inhibiting soluble CX3 CL1 formation. Additionally, Tat-CX3 CL1(357–395 aa) attenuated long-term cognitive deficits and improved white matter integrity as determined by the Morris water maze test at 31–34 days following surgery and immunofluorescence staining at 35 days after stroke, respectively. In conclusion, Tat-CX3 CL1(357–395 aa) facilitates functional recovery after ischemic stroke by promoting microglial polarization from M1 to M2. Therefore, the Tat-CX3 CL1(357–395 aa) is a potential therapeutic agent for ischemic stroke.展开更多
文摘To address the issues of reduced performance and shortened lifespan during the low-carbonizating process of Al_(2)O_(3)-C refractories,nano-crystalline ZrC modified graphite was prepared using Zr powder and flake graphite as raw materials,with NaCl and NaF mixed salt serving as the medium.The flake graphite was gradually replaced by ZrC modified graphite in the preparation of Al_(2)O_(3)-C refractories,and its impact on the material’s structure and properties was investigated.The results indicate that,compared to samples with only flake graphite,the introduction of 1 mass%to 5 mass%nano-crystalline ZrC modified graphite can significantly enhance the mechanical performance of low-carbon Al_(2)O_(3)-C refractories.When 5 mass%ZrC modified graphite is added,the mechanical properties of the samples are optimal,with the cold modulus of rupture and elastic modulus reaching 22.5 MPa and 65.0 GPa,respectively.
基金supported by the National Natural Science Foundation of China,Nos. 82071304 (to QXZ), 81671149 (to QXZ),and 81971179 (to XML)the Natural Science Foundation of Jiangsu Province,Nos. BK20191463 (to XML) and BK20161167 (to QXZ)。
文摘We previously reported that postsynaptic density-93 mediates neuron-microglia crosstalk by interacting with amino acids 357–395 of C-X3-C motif chemokine ligand 1(CX3 CL1) to induce microglia polarization. More importantly, the peptide Tat-CX3 CL1(comprising amino acids 357–395 of CX3 CL1) disrupts the interaction between postsynaptic density-93 and CX3 CL1, reducing neurological impairment and exerting a protective effect in the context of acute ischemic stroke. However, the mechanism underlying these effects remains unclear. In the current study, we found that the pro-inflammatory M1 phenotype increased and the anti-inflammatory M2 phenotype decreased at different time points. The M1 phenotype increased at 6 hours after stroke and peaked at 24 hours after perfusion, whereas the M2 phenotype decreased at 6 and 24 hours following reperfusion. We found that the peptide Tat-CX3 CL1(357–395 aa) facilitates microglial polarization from M1 to M2 by reducing the production of soluble CX3 CL1. Furthermore, the a disintegrin and metalloprotease domain 17(ADAM17) inhibitor GW280264 x, which inhibits metalloprotease activity and prevents CX3 CL1 from being sheared into its soluble form, facilitated microglial polarization from M1 to M2 by inhibiting soluble CX3 CL1 formation. Additionally, Tat-CX3 CL1(357–395 aa) attenuated long-term cognitive deficits and improved white matter integrity as determined by the Morris water maze test at 31–34 days following surgery and immunofluorescence staining at 35 days after stroke, respectively. In conclusion, Tat-CX3 CL1(357–395 aa) facilitates functional recovery after ischemic stroke by promoting microglial polarization from M1 to M2. Therefore, the Tat-CX3 CL1(357–395 aa) is a potential therapeutic agent for ischemic stroke.
