A preparation technology of MgO powder used in special silicon steel from hydromagnesite mineral has been developed. The preparation technology includes the following steps： （1） calcining the hydromagnesite at 700-...A preparation technology of MgO powder used in special silicon steel from hydromagnesite mineral has been developed. The preparation technology includes the following steps： （1） calcining the hydromagnesite at 700-750°C for 1.5-2 h; （2） hydrating the calcined hydromagnesite to be slurry containing the solid-liquid ratio of 15-20 g？L？1; （3） acquiring Mg（HCO3）2 solution by carbonating the slurry, the carbonation temperature, CO2 pressure, and end point PH value of carbonation are less than 40°C, 0.4-0.6 MPa, and 7 respectively during the carbonation process; （4） preparing precipitated basic magnesium carbonate by thermally decomposing the Mg（HCO3）2 solution at 90-100°C; （5） obtaining the MgO product by calcining the precipitated basic magnesium carbonate at 850-950°C for 30-60 min, and adopting flowing nitrogen during the cooling process. By using this technology, more than 80wt% magnesium in hydromagnesite mineral can be extracted, and high-performance MgO products used in special silicon steel can be ob- tained.展开更多
The present study assessed the influence of medium-intensity （treadmill at a speed of 19.3 m/min until exhaustion） and high-intensity （treadmill at a speed of 26.8 m/min until exhaustion） acute exhaustive exercise...The present study assessed the influence of medium-intensity （treadmill at a speed of 19.3 m/min until exhaustion） and high-intensity （treadmill at a speed of 26.8 m/min until exhaustion） acute exhaustive exercise on rat hippocampal neural cell apoptosis. TUNEL staining showed significantly increased neural cell apoptosis in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise, particulady the medium-intensity acute exhaustive exercise, when compared with the control. Immunohistochemistry showed significantly increased expression of the antiapoptotic protein Bcl-2 and the proapoptotJc proteJn Bax in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise. Additionally, the ratio of Bax to Bcl-2 increased in both exercise groups. In particular, the medium-intensity acute exhaustive exercise group had significantly higher Bax and Bcl-2 protein expression and a higher Bax/Bcl-2 ratio. These findings indicate that acute exhaustive exercise of different intensities can induce neural cell apoptosis in the hippocampus, and that medium-intensity acute exhaustive exercise results in greater damage when compared with high-intensity exercise.展开更多
The ORF9b protein,derived from the nucleocapsid’s open-reading frame in both SARS-CoV and SARS-CoV-2,serves as an accessory protein crucial for viral immune evasion by inhibiting the innate immune response.Despite it...The ORF9b protein,derived from the nucleocapsid’s open-reading frame in both SARS-CoV and SARS-CoV-2,serves as an accessory protein crucial for viral immune evasion by inhibiting the innate immune response.Despite its significance,the precise regulatory mechanisms underlying its function remain elusive.In the present study,we unveil that the ORF9b protein of SARS-CoV-2,including emerging mutant strains like Delta and Omicron,can undergo ubiquitination at the K67 site and subsequent degradation via the proteasome pathway,despite certain mutations present among these strains.Moreover,our investigation further uncovers the pivotal role of the translocase of the outer mitochondrial membrane 70(TOM70)as a substrate receptor,bridging ORF9b with heat shock protein 90 alpha(HSP90α)and Cullin 5(CUL5)to form a complex.Within this complex,CUL5 triggers the ubiquitination and degradation of ORF9b,acting as a host antiviral factor,while HSP90αfunctions to stabilize it.Notably,treatment with HSP90 inhibitors such as GA or 17-AAG accelerates the degradation of ORF9b,leading to a pronounced inhibition of SARS-CoV-2 replication.Single-cell sequencing data revealed an up-regulation of HSP90αin lung epithelial cells from COVID-19 patients,suggesting a potential mechanism by which SARS-CoV-2 may exploit HSP90αto evade the host immunity.Our study identifies the CUL5-TOM70-HSP90αcomplex as a critical regulator of ORF9b protein stability,shedding light on the intricate host–virus immune response dynamics and offering promising avenues for drug development against SARS-CoV-2 in clinical settings.展开更多
基金the Science and Technology Program Project of Hunan Province, China (No.06SK2011).
文摘A preparation technology of MgO powder used in special silicon steel from hydromagnesite mineral has been developed. The preparation technology includes the following steps： （1） calcining the hydromagnesite at 700-750°C for 1.5-2 h; （2） hydrating the calcined hydromagnesite to be slurry containing the solid-liquid ratio of 15-20 g？L？1; （3） acquiring Mg（HCO3）2 solution by carbonating the slurry, the carbonation temperature, CO2 pressure, and end point PH value of carbonation are less than 40°C, 0.4-0.6 MPa, and 7 respectively during the carbonation process; （4） preparing precipitated basic magnesium carbonate by thermally decomposing the Mg（HCO3）2 solution at 90-100°C; （5） obtaining the MgO product by calcining the precipitated basic magnesium carbonate at 850-950°C for 30-60 min, and adopting flowing nitrogen during the cooling process. By using this technology, more than 80wt% magnesium in hydromagnesite mineral can be extracted, and high-performance MgO products used in special silicon steel can be ob- tained.
基金supported by the National Natural Science Foundation of China, No. 30500269
文摘The present study assessed the influence of medium-intensity （treadmill at a speed of 19.3 m/min until exhaustion） and high-intensity （treadmill at a speed of 26.8 m/min until exhaustion） acute exhaustive exercise on rat hippocampal neural cell apoptosis. TUNEL staining showed significantly increased neural cell apoptosis in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise, particulady the medium-intensity acute exhaustive exercise, when compared with the control. Immunohistochemistry showed significantly increased expression of the antiapoptotic protein Bcl-2 and the proapoptotJc proteJn Bax in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise. Additionally, the ratio of Bax to Bcl-2 increased in both exercise groups. In particular, the medium-intensity acute exhaustive exercise group had significantly higher Bax and Bcl-2 protein expression and a higher Bax/Bcl-2 ratio. These findings indicate that acute exhaustive exercise of different intensities can induce neural cell apoptosis in the hippocampus, and that medium-intensity acute exhaustive exercise results in greater damage when compared with high-intensity exercise.
基金supported by the National Key Research and Development Program of China(2021YFC2300103)the National Natural Science Foundation of China(U21A20384 and 82072293)+1 种基金the Natural Science Foundation of Hunan Province,China(2022JJ30692)the China Postdoctoral Science Foundation(2023M731520).
文摘The ORF9b protein,derived from the nucleocapsid’s open-reading frame in both SARS-CoV and SARS-CoV-2,serves as an accessory protein crucial for viral immune evasion by inhibiting the innate immune response.Despite its significance,the precise regulatory mechanisms underlying its function remain elusive.In the present study,we unveil that the ORF9b protein of SARS-CoV-2,including emerging mutant strains like Delta and Omicron,can undergo ubiquitination at the K67 site and subsequent degradation via the proteasome pathway,despite certain mutations present among these strains.Moreover,our investigation further uncovers the pivotal role of the translocase of the outer mitochondrial membrane 70(TOM70)as a substrate receptor,bridging ORF9b with heat shock protein 90 alpha(HSP90α)and Cullin 5(CUL5)to form a complex.Within this complex,CUL5 triggers the ubiquitination and degradation of ORF9b,acting as a host antiviral factor,while HSP90αfunctions to stabilize it.Notably,treatment with HSP90 inhibitors such as GA or 17-AAG accelerates the degradation of ORF9b,leading to a pronounced inhibition of SARS-CoV-2 replication.Single-cell sequencing data revealed an up-regulation of HSP90αin lung epithelial cells from COVID-19 patients,suggesting a potential mechanism by which SARS-CoV-2 may exploit HSP90αto evade the host immunity.Our study identifies the CUL5-TOM70-HSP90αcomplex as a critical regulator of ORF9b protein stability,shedding light on the intricate host–virus immune response dynamics and offering promising avenues for drug development against SARS-CoV-2 in clinical settings.
