Sweet potatoes are significant cash crops,however,their yield and quality are greatly compromised by viral diseases.In this study,the complete genomic sequences of two Sweet Potato Virus 2(SPV2)isolates from infected ...Sweet potatoes are significant cash crops,however,their yield and quality are greatly compromised by viral diseases.In this study,the complete genomic sequences of two Sweet Potato Virus 2(SPV2)isolates from infected sweet potato leaves in the Shandong(designated as SPV2-SDYT,GenBank No.PQ855660.1)and Jiangsu(designated as SPV2-JSXZ,GenBank No.PQ855661.1)provinces in China were obtained using 5′RACE and RT-PCR amplification.Consistency,phylogeny,codon usage bias,recombination,and selection pressure analyses were conducted using the SPV2-SDYT and SPV2-JSXZ genome sequences.The complete genome sequences of SPV2-SDYT and SPV2-JSXZ were 10561 nucleotides(nt)in length,with respective nucleotide and amino acid identities of 99.25%and 99.12%,respectively.Both isolates were closely related to the SPV2 isolate from China(SPV2-LN).In both SPV2-SDYT and SPV2-JSXZ,the identity of the P1 protein was the highest,whereas that of the P3 protein was the lowest.There were 26 codons with relatively synonymous codon usage(RSCU)values greater than 1 in SPV2-SDYT and 27 codons with RSCU values greater than 1 in SPV2-JSXZ.High-frequency codons in their genomes were predominantly found to end with A/U.Recombination analysis revealed no major recombination sites in either SPV2-SDYT or SPV2-JSXZ.Further selection pressure analysis showed that the non-synonymous substitution rate/synonymous substitution rate(dN/dS)value of all 10 SPV2 proteins was less than 1.This is the first report on the evolutionary relationships of the 17 known SPV2 isolates.Our findings lay the molecular groundwork for preventing and controlling SPV2 infection in root-tuber crops.These findings also contribute to our understanding of the spread and evolution of SPV2,its pathogenic mechanisms,and the development of antiviral strategies against it.展开更多
Carbon dioxide embolism is a rare but severe complication of laparoscopic hepatectomy.We reported a case of massive carbon dioxide embolism that developed into a rare paradoxical gas embolism during laparoscopic hepat...Carbon dioxide embolism is a rare but severe complication of laparoscopic hepatectomy.We reported a case of massive carbon dioxide embolism that developed into a rare paradoxical gas embolism during laparoscopic hepatectomy and resulted in reduced muscular power of the left upper extremity,severe pleural effusion and hypoalbuminemia after surgery.Fortunately,the patient fully recovered with positive prevention and postoperative treatment.This case report highlights that the surgeon and anaesthesiologist must be aware of the risks and the importance for prompt treatment when massive carbon dioxide embolism occurs.展开更多
This study reports several modification strategies to optimize and enhance the performance of twodimensional(2D) metal organic frameworks(MOFs)-derived catalysts in peroxydisulfate(PDS) activation.The raw 2D Ni-MOF an...This study reports several modification strategies to optimize and enhance the performance of twodimensional(2D) metal organic frameworks(MOFs)-derived catalysts in peroxydisulfate(PDS) activation.The raw 2D Ni-MOF and 2D Ni-Fe-MOF without modification show poor catalytic activities for PDS activation and high metal ion leaching. The carbonization of 2D MOF can increase the activity of the catalyst but cannot solve the metal leaching problem. The further acid treatment of carbonization products can further improve the catalytic activity and decrease the metal ion leaching. The in-situ growth of2D MOF on graphene oxide(GO) support with subsequent carbonization and acid treatment offers the best performance in PDS activation for organic pollutant removal with low metal ion leaching. Compared with other PDS systems, the Ni-Fe-C-acid/GO system displays much lower catalyst and PDS dosages for p-chloroaniline degradation. This study presents new insights in the modification strategies of 2D MOFbased catalysts in PDS activation.展开更多
Energy status is linked to the production of reactive oxygen species(ROS)in macrophages,which is elevated in obesity.However,it is unclear how ROS production is upregulated in macrophages in response to energy overloa...Energy status is linked to the production of reactive oxygen species(ROS)in macrophages,which is elevated in obesity.However,it is unclear how ROS production is upregulated in macrophages in response to energy overload for mediating the development of obesity.Here,we show that the Rab-GTPase activating protein(Rab GAP)TBC1D1,a substrate of the energy sensor AMP-activated protein kinase(AMPK),is a critical regulator of macrophage ROS production and consequent adipose inflammation for obesity development.TBC1D1 deletion decreases,whereas an energy overload-mimetic non-phosphorylatable TBC1D1^(S231A)Amutation increases,ROS production and M1-like polarization in macrophages.Mechanistically,TBC1D1 and its downstream target Rab8a form an energy-responsive complex with NOX2 for ROS generation.Transplantation of TBC1D1^(S231A)bone marrow aggravates diet-induced obesity whereas treatment with an ultra-stable Tt SOD for removal of ROS selectively in macrophages alleviates both TBC1D1~(S231A)mutation-and diet-induced obesity.Our findings therefore have implications for drug discovery to combat obesity.展开更多
Diabetic cardiomyopathy(DCM)is currently a progressive and nonstoppable complication in type 2 diabetic patients.Metabolic insults and insulin resistance are involved in its pathogenesis;however,the underlying mechani...Diabetic cardiomyopathy(DCM)is currently a progressive and nonstoppable complication in type 2 diabetic patients.Metabolic insults and insulin resistance are involved in its pathogenesis;however,the underlying mechanisms are still not clearly understood.Here we show that calcium dysregulation can be both a cause and a consequence of cardiac insulin resistance that leads to DCM.A western diet induces the development of DCM through at least three phases in mice,among which an early phase depends on impaired Thr^(484)-phosphorylation of sarcoplasmic/endoplasmic reticulum calcium ATPase 2a(SERCA2a)elicited by insulin resistance.Mutation of SERCA2a-Thr^(484)to a nonphosphorylatable alanine delays calcium re-uptake into the sarcoplasmic reticulum in the cardiomyocytes and decreases cardiac function at the baseline.Importantly,this mutation blunts the early phase of DCM,but has no effect on disease progression in the following phases.Interestingly,impairment of sarcoplasmic reticulum calcium re-uptake caused by the SERCA2a-Thr^(484)mutation inhibited processing of insulin receptor precursor through FURIN convertase,resulting in cardiac insulin resistance.Collectively,these data reveal a bidirectional relationship between insulin resistance and impairment of calcium homeostasis,which may underlie the early pathogenesis of DCM.Our findings have therapeutic implications for early intervention of DCM.展开更多
基金Funding Statement:This work was funded by the National Natural Science Foundation of China(32100132)Shandong Province Natural Sciences Foundation of China(ZR2021QC008)+1 种基金Youth Innovation Team Program'in College of Shandong Province of China(2022KJ119)supported by Young Talent of Lifting Engineering for Science and Technology in Shandong,China(SDAST2024QT085).
文摘Sweet potatoes are significant cash crops,however,their yield and quality are greatly compromised by viral diseases.In this study,the complete genomic sequences of two Sweet Potato Virus 2(SPV2)isolates from infected sweet potato leaves in the Shandong(designated as SPV2-SDYT,GenBank No.PQ855660.1)and Jiangsu(designated as SPV2-JSXZ,GenBank No.PQ855661.1)provinces in China were obtained using 5′RACE and RT-PCR amplification.Consistency,phylogeny,codon usage bias,recombination,and selection pressure analyses were conducted using the SPV2-SDYT and SPV2-JSXZ genome sequences.The complete genome sequences of SPV2-SDYT and SPV2-JSXZ were 10561 nucleotides(nt)in length,with respective nucleotide and amino acid identities of 99.25%and 99.12%,respectively.Both isolates were closely related to the SPV2 isolate from China(SPV2-LN).In both SPV2-SDYT and SPV2-JSXZ,the identity of the P1 protein was the highest,whereas that of the P3 protein was the lowest.There were 26 codons with relatively synonymous codon usage(RSCU)values greater than 1 in SPV2-SDYT and 27 codons with RSCU values greater than 1 in SPV2-JSXZ.High-frequency codons in their genomes were predominantly found to end with A/U.Recombination analysis revealed no major recombination sites in either SPV2-SDYT or SPV2-JSXZ.Further selection pressure analysis showed that the non-synonymous substitution rate/synonymous substitution rate(dN/dS)value of all 10 SPV2 proteins was less than 1.This is the first report on the evolutionary relationships of the 17 known SPV2 isolates.Our findings lay the molecular groundwork for preventing and controlling SPV2 infection in root-tuber crops.These findings also contribute to our understanding of the spread and evolution of SPV2,its pathogenic mechanisms,and the development of antiviral strategies against it.
基金This work was supported by the Medicine and Health Science and Technology Project of Zhejiang Province,China(2018277726).
文摘Carbon dioxide embolism is a rare but severe complication of laparoscopic hepatectomy.We reported a case of massive carbon dioxide embolism that developed into a rare paradoxical gas embolism during laparoscopic hepatectomy and resulted in reduced muscular power of the left upper extremity,severe pleural effusion and hypoalbuminemia after surgery.Fortunately,the patient fully recovered with positive prevention and postoperative treatment.This case report highlights that the surgeon and anaesthesiologist must be aware of the risks and the importance for prompt treatment when massive carbon dioxide embolism occurs.
基金supported by the National Key R&D Program of China (No. 2019YFC1905400)。
文摘This study reports several modification strategies to optimize and enhance the performance of twodimensional(2D) metal organic frameworks(MOFs)-derived catalysts in peroxydisulfate(PDS) activation.The raw 2D Ni-MOF and 2D Ni-Fe-MOF without modification show poor catalytic activities for PDS activation and high metal ion leaching. The carbonization of 2D MOF can increase the activity of the catalyst but cannot solve the metal leaching problem. The further acid treatment of carbonization products can further improve the catalytic activity and decrease the metal ion leaching. The in-situ growth of2D MOF on graphene oxide(GO) support with subsequent carbonization and acid treatment offers the best performance in PDS activation for organic pollutant removal with low metal ion leaching. Compared with other PDS systems, the Ni-Fe-C-acid/GO system displays much lower catalyst and PDS dosages for p-chloroaniline degradation. This study presents new insights in the modification strategies of 2D MOFbased catalysts in PDS activation.
基金the Ministry of Science and Technology of China(Grant Nos.2018YFA0801100 and 2021YFF0702100)the National Natural Science Foundation of China(Grant Nos.32025019 and 31970719 to S.C.,31971067)the Fundamental Research Funds for the Central Universities(021414380533,021414380505)for financial support。
文摘Energy status is linked to the production of reactive oxygen species(ROS)in macrophages,which is elevated in obesity.However,it is unclear how ROS production is upregulated in macrophages in response to energy overload for mediating the development of obesity.Here,we show that the Rab-GTPase activating protein(Rab GAP)TBC1D1,a substrate of the energy sensor AMP-activated protein kinase(AMPK),is a critical regulator of macrophage ROS production and consequent adipose inflammation for obesity development.TBC1D1 deletion decreases,whereas an energy overload-mimetic non-phosphorylatable TBC1D1^(S231A)Amutation increases,ROS production and M1-like polarization in macrophages.Mechanistically,TBC1D1 and its downstream target Rab8a form an energy-responsive complex with NOX2 for ROS generation.Transplantation of TBC1D1^(S231A)bone marrow aggravates diet-induced obesity whereas treatment with an ultra-stable Tt SOD for removal of ROS selectively in macrophages alleviates both TBC1D1~(S231A)mutation-and diet-induced obesity.Our findings therefore have implications for drug discovery to combat obesity.
基金Thanks to the Ministry of Science and Technology of China(Grant Nos.2018YFA0801100 and 2021YFF0702100 to H.-Y.W.and S.C.)the National Natural Science Foundation of China(Grant Nos.32025019 and 31970719 to S.C.,82000349 to C.Q.,32000800 to M.L.,82000736 to Q.C.,and 31971067 to H.-Y.W.)+1 种基金the Science and Technology Foundation of Jiangsu Province of China(Grant Nos.BK20200315(Basic Research Program)to C.Q.and BK20190305(Basic Research Program)to Q.C.)the Fundamental Research Funds for the Central Universities(Grant Nos.021414380524 to S.C.,021414380508 to C.Q.,and 021414380505 to Q.C.),for financial support.
文摘Diabetic cardiomyopathy(DCM)is currently a progressive and nonstoppable complication in type 2 diabetic patients.Metabolic insults and insulin resistance are involved in its pathogenesis;however,the underlying mechanisms are still not clearly understood.Here we show that calcium dysregulation can be both a cause and a consequence of cardiac insulin resistance that leads to DCM.A western diet induces the development of DCM through at least three phases in mice,among which an early phase depends on impaired Thr^(484)-phosphorylation of sarcoplasmic/endoplasmic reticulum calcium ATPase 2a(SERCA2a)elicited by insulin resistance.Mutation of SERCA2a-Thr^(484)to a nonphosphorylatable alanine delays calcium re-uptake into the sarcoplasmic reticulum in the cardiomyocytes and decreases cardiac function at the baseline.Importantly,this mutation blunts the early phase of DCM,but has no effect on disease progression in the following phases.Interestingly,impairment of sarcoplasmic reticulum calcium re-uptake caused by the SERCA2a-Thr^(484)mutation inhibited processing of insulin receptor precursor through FURIN convertase,resulting in cardiac insulin resistance.Collectively,these data reveal a bidirectional relationship between insulin resistance and impairment of calcium homeostasis,which may underlie the early pathogenesis of DCM.Our findings have therapeutic implications for early intervention of DCM.
