Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion(IR) injury and apoptosis in rat.Methods Wistar rats were randomly assigned to four groups:sham group...Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion(IR) injury and apoptosis in rat.Methods Wistar rats were randomly assigned to four groups:sham group(n =6):no ischaemia-reperfusion;IR group(n =6):left lung ischemia was achieved by clamping the hilum for 90 min,followed by 120 min reperfusion;sev+pre group(n =6):1 minimum alveolar concentration(MAC) sevoflurane was admi-nistered for 30 min prior to ischemia;sev+post group(n =6):ischemia was followed by 1 MAC sevoflurane postconditioning at the first 30 min reperfusion.PaO2 was measured after reperfusion.The number of apoptotic cells was estimated using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling(TUNEL) technique.Results After ischemia-reperfusion,a significant deterioration of PaO2 was noticed and the number of apoptotic cells remarkably increased compared with that of sham group.In sev+pre group and sev+post group,PaO2 was(85.7±14.4) mmHg and(88.6±12.5) mmHg respectively,which was apparently increased compared with that in IR group [(63.9±11.3) mmHg,P <0.05].The number of apoptotic cells in sev+pre group [(6.94 ± 1.49)%] and sev+post group [(7.69 ± 1.61)%] was significantly lower than that in IR group [(12.12 ± 2.77)%,P <0.05].But all parameters showed no significant difference between sev+pre group and sev+post group.Conclusions Both sevoflurane preconditioning and postconditioning could prevent lung ischemia-reperfusion injury and attenuate apoptosis in rat.展开更多
While some individuals infected by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)present mild-to-severe disease,many SARS-CoV-2-infected individuals are asymptomatic.We sought to identify the distinction ...While some individuals infected by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)present mild-to-severe disease,many SARS-CoV-2-infected individuals are asymptomatic.We sought to identify the distinction of immune response between asymptomatic and moderate patients.We performed single-cell transcriptome and T-cell/B-cell receptor(TCR/BCR)sequencing in 37 longitudinal collected peripheral blood mononuclear cell samples from asymptomatic,moderate,and severe patients with healthy controls.Asymptomatic patients displayed increased CD56^(bri)CD16^(-) natural killer(NK)cells and upregulation of interferon-gamma in effector CD4^(+) and CD8^(+) T cells and NK cells.They showed more robust TCR clonal expansion,especially in effector CD4^(+) T cells,but lack strong BCR clonal expansion compared to moderate patients.Moreover,asymptomatic patients have lower interferon-stimulated genes(ISGs)expression in general but large interpatient variability,whereas moderate patients showed various magnitude and temporal dynamics of the ISGs expression across multiple cell populations but lower than a patient with severe disease.Our data provide evidenee of different immune signatures to SARS-CoV-2 in asymptomatic infections.展开更多
文摘Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion(IR) injury and apoptosis in rat.Methods Wistar rats were randomly assigned to four groups:sham group(n =6):no ischaemia-reperfusion;IR group(n =6):left lung ischemia was achieved by clamping the hilum for 90 min,followed by 120 min reperfusion;sev+pre group(n =6):1 minimum alveolar concentration(MAC) sevoflurane was admi-nistered for 30 min prior to ischemia;sev+post group(n =6):ischemia was followed by 1 MAC sevoflurane postconditioning at the first 30 min reperfusion.PaO2 was measured after reperfusion.The number of apoptotic cells was estimated using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling(TUNEL) technique.Results After ischemia-reperfusion,a significant deterioration of PaO2 was noticed and the number of apoptotic cells remarkably increased compared with that of sham group.In sev+pre group and sev+post group,PaO2 was(85.7±14.4) mmHg and(88.6±12.5) mmHg respectively,which was apparently increased compared with that in IR group [(63.9±11.3) mmHg,P <0.05].The number of apoptotic cells in sev+pre group [(6.94 ± 1.49)%] and sev+post group [(7.69 ± 1.61)%] was significantly lower than that in IR group [(12.12 ± 2.77)%,P <0.05].But all parameters showed no significant difference between sev+pre group and sev+post group.Conclusions Both sevoflurane preconditioning and postconditioning could prevent lung ischemia-reperfusion injury and attenuate apoptosis in rat.
基金supported by grants from the Beijing Natural Science Foundation(L202038)the Natural Science Foundation of China(81773494,81621005)the Emergency Science and Technology Project for Prevention and Control of COVID-19(20277734D).
文摘While some individuals infected by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)present mild-to-severe disease,many SARS-CoV-2-infected individuals are asymptomatic.We sought to identify the distinction of immune response between asymptomatic and moderate patients.We performed single-cell transcriptome and T-cell/B-cell receptor(TCR/BCR)sequencing in 37 longitudinal collected peripheral blood mononuclear cell samples from asymptomatic,moderate,and severe patients with healthy controls.Asymptomatic patients displayed increased CD56^(bri)CD16^(-) natural killer(NK)cells and upregulation of interferon-gamma in effector CD4^(+) and CD8^(+) T cells and NK cells.They showed more robust TCR clonal expansion,especially in effector CD4^(+) T cells,but lack strong BCR clonal expansion compared to moderate patients.Moreover,asymptomatic patients have lower interferon-stimulated genes(ISGs)expression in general but large interpatient variability,whereas moderate patients showed various magnitude and temporal dynamics of the ISGs expression across multiple cell populations but lower than a patient with severe disease.Our data provide evidenee of different immune signatures to SARS-CoV-2 in asymptomatic infections.