Background:Aeromedical evacuation of patients with burn trauma is an important transport method in times of peace and war,during which patients are exposed to prolonged periods of hypobaric hypoxia;however,the effects...Background:Aeromedical evacuation of patients with burn trauma is an important transport method in times of peace and war,during which patients are exposed to prolonged periods of hypobaric hypoxia;however,the effects of such exposure on burn injuries,particularly on burn-induced lung injuries,are largely unexplored.This study aimed to determine the effects of hypobaric hypoxia on burn-induced lung injuries and to investigate the underlying mechanism using a rat burn model.Methods:A total of 40 male Wistar rats were randomly divided into four groups(10 in each group):sham burn(SB)group,burn in normoxia condition(BN)group,burn in hypoxia condition(BH)group,and burn in hypoxia condition with treatment intervention(BHD)group.Rats with 30%total body surface area burns were exposed to hypobaric hypoxia(2000 m altitude simulation)or normoxia conditions for 4 h.Deoxyribonuclease I(DNase I)was administered systemically as a treatment intervention.Systemic inflammatory mediator and mitochondrial deoxyribonucleic acid(mtDNA)levels were determined.A histopathological evaluation was performed and the acute lung injury(ALI)score was determined.Malonaldehyde(MDA)content,myeloperoxidase(MPO)activity,and the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3)inflammasome level were determined in lung tissues.Data among groups were compared using analysis of variance followed by Tukey’s test post hoc analysis.Results:Burns resulted in a remarkably higher level of systemic inflammatory cytokines and mtDNA release,which was further heightened by hypobaric hypoxia exposure(P<0.01).Moreover,hypobaric hypoxia exposure gave rise to increased NLRP3 inflammasome expression,MDA content,and MPO activity in the lung(P<0.05 or P<0.01).Burn-induced lung injuries were exacerbated,as shown by the histopathological evaluation and ALI score(P<0.01).Administration of DNase I markedly reduced mtDNA release and systemic inflammatory cytokine production.Furthermore,the NLRP3 inflammasome level in lung tissues was decreased and burn-induced lung injury was ameliorated(P<0.01).Conclusions:Our results suggested that simulated aeromedical evacuation further increased burn-induced mtDNA release and exacerbated burn-induced inflammation and lung injury.DNase I reduced the release of mtDNA,limited mtDNA-induced systemic inflammation,and ameliorated burn-induced ALI.The intervening mtDNA level is thus a potential target to protect from burn-induced lung injury during aeromedical conditions and provides safer air evacuations for severely burned patients.展开更多
The impacts of HfOx inserting layer thickness on the electrical properties of the ZnO-based transparent resistance random access memory （TRRAM） device were investigated in this paper. The bipolar resistive switching...The impacts of HfOx inserting layer thickness on the electrical properties of the ZnO-based transparent resistance random access memory （TRRAM） device were investigated in this paper. The bipolar resistive switching behavior of a single ZnO film and bilayer HfOx/ZnO films as active layers for TRRAM devices was demonstrated. It was revealed that the bilayer TRRAM device with a 10-nm HfOx inserted layer had a more stable resistive switching behavior than other devices including the single layer device, as well as being forming free, and the transmittance was more than 80% in the visible region. For the HfOx/ZnO devices, the current conduction behavior was dominated by the space-charge-limited current mechanism in the low resistive state （LRS） and Schottky emission in the high resistive state （HRS）, while the mechanism for single layer devices was controlled by ohmic conduction in the LRS and Poole-Frenkel emission in the HRS.展开更多
基金supported by the Youth Incubation Project from the Sanitary Bureau of Logistics Security Ministry of the Central Military Commission(19QNP025)Major Applied Basic Research Project from the Logistics Security Ministry of the Central Military Commission(AKJ15J001)。
文摘Background:Aeromedical evacuation of patients with burn trauma is an important transport method in times of peace and war,during which patients are exposed to prolonged periods of hypobaric hypoxia;however,the effects of such exposure on burn injuries,particularly on burn-induced lung injuries,are largely unexplored.This study aimed to determine the effects of hypobaric hypoxia on burn-induced lung injuries and to investigate the underlying mechanism using a rat burn model.Methods:A total of 40 male Wistar rats were randomly divided into four groups(10 in each group):sham burn(SB)group,burn in normoxia condition(BN)group,burn in hypoxia condition(BH)group,and burn in hypoxia condition with treatment intervention(BHD)group.Rats with 30%total body surface area burns were exposed to hypobaric hypoxia(2000 m altitude simulation)or normoxia conditions for 4 h.Deoxyribonuclease I(DNase I)was administered systemically as a treatment intervention.Systemic inflammatory mediator and mitochondrial deoxyribonucleic acid(mtDNA)levels were determined.A histopathological evaluation was performed and the acute lung injury(ALI)score was determined.Malonaldehyde(MDA)content,myeloperoxidase(MPO)activity,and the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3)inflammasome level were determined in lung tissues.Data among groups were compared using analysis of variance followed by Tukey’s test post hoc analysis.Results:Burns resulted in a remarkably higher level of systemic inflammatory cytokines and mtDNA release,which was further heightened by hypobaric hypoxia exposure(P<0.01).Moreover,hypobaric hypoxia exposure gave rise to increased NLRP3 inflammasome expression,MDA content,and MPO activity in the lung(P<0.05 or P<0.01).Burn-induced lung injuries were exacerbated,as shown by the histopathological evaluation and ALI score(P<0.01).Administration of DNase I markedly reduced mtDNA release and systemic inflammatory cytokine production.Furthermore,the NLRP3 inflammasome level in lung tissues was decreased and burn-induced lung injury was ameliorated(P<0.01).Conclusions:Our results suggested that simulated aeromedical evacuation further increased burn-induced mtDNA release and exacerbated burn-induced inflammation and lung injury.DNase I reduced the release of mtDNA,limited mtDNA-induced systemic inflammation,and ameliorated burn-induced ALI.The intervening mtDNA level is thus a potential target to protect from burn-induced lung injury during aeromedical conditions and provides safer air evacuations for severely burned patients.
基金Project supported by the National Key Research and Development Program of China(Grant No.2017yfb0405600)the National Natural Science Foundation of China(Grant Nos.61404091,61274113,61505144,51502203,and 51502204)the Natural Science Foundation of Tianjin City(Grant Nos.17JCYBJC16100 and 17JCZDJC31700)
文摘The impacts of HfOx inserting layer thickness on the electrical properties of the ZnO-based transparent resistance random access memory （TRRAM） device were investigated in this paper. The bipolar resistive switching behavior of a single ZnO film and bilayer HfOx/ZnO films as active layers for TRRAM devices was demonstrated. It was revealed that the bilayer TRRAM device with a 10-nm HfOx inserted layer had a more stable resistive switching behavior than other devices including the single layer device, as well as being forming free, and the transmittance was more than 80% in the visible region. For the HfOx/ZnO devices, the current conduction behavior was dominated by the space-charge-limited current mechanism in the low resistive state （LRS） and Schottky emission in the high resistive state （HRS）, while the mechanism for single layer devices was controlled by ohmic conduction in the LRS and Poole-Frenkel emission in the HRS.
