Reduction kinetics and carbon deposit for Cu-doped Fe-based oxygen carriers: role of Cu

2021 ◽  
pp. 117406
Guida Li ◽  
Wenxing Yao ◽  
Yunlei Zhao ◽  
Bo Jin ◽  
Jianyong Xu ◽  
2007 ◽  
Vol 128 ◽  
pp. 249-254 ◽  
Urszula Narkiewicz ◽  
Marcin Podsiadły ◽  
Iwona Pełech ◽  
Waleran Arabczyk ◽  
M.J. Woźniak ◽  

Nanocrystalline cobalt was carburised with ethylene in the range 340– 500°C to obtain Co(C) nanocapsules. The carbon deposit was reduced by a flow of hydrogen in the range 500– 560°C. The reduction kinetics were studied using thermogravimetry, described by the equation: α = Α[1-exp(-kt)n]. The apparent activation energy of the reduction process of the carbon deposit was determined. After carburisation and reduction the samples were examined by XRD and HRTEM.

2002 ◽  
Vol 30 (1) ◽  
pp. 39-51 ◽  
Scott C. Dorman ◽  
Clare F. Kenny ◽  
Lee Miller ◽  
Rhoda Elison Hirsch ◽  
John P. Harrington

2009 ◽  
Vol 33 (2) ◽  
pp. 127-132 ◽  
Fumiaki Yoshiba ◽  
Akira T. Kawaguchi ◽  
Osamu Hyodo ◽  
Takaaki Kinoue ◽  
Sadaki Inokuchi ◽  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Bonpei Takase ◽  
Yuko Higashimura ◽  
Yoshihiro Tanaka ◽  
Kenichi Hashmoto

Lethal ventricular arrhythmias (VT/VF) are serious complications after resuscitation of severe hemorrhagic shock (HS). To investigate mechanisms of arrhythmogenesis after HS and a role of two different concentration of oxygenated liposome-encapsulated human hemoglobin (LHb [Hgb=6g] or HbV [Hgb=10g]), optical mapping analysis (OMP) and electrophysiological study (EPS) were performed using rat HS model. HS was induced by withdrawing 30% blood from aorta (shock alone). Rats were resuscitated by transfusing saline, 5% albumin (5%ALB), LHb, HbV or oxygenated autologous washed red blood cells (wRBC: n=7, per group). After excising heart, OMP and EPS were performed in isolated Langendorff-perfused hearts. OMP revealed abnormal ventricular conduction delay (VCD) with impaired action potential duration dispersion (APDd) in both ventricles in shock alone, saline, and 5%ALB whereas VCD and APDd were substantially attenuated in LHb, HbV or wRBC (a). VT/VF was easily provoked by burst pacing stimulus to LV in saline and 5%ALB while few VT/VF was induced in LHb, LbV or wRBC (b). Conclusion: Ventricular electrical remodeling of abnormal VCD and APDd after HS causes VT/VF. LHb, LbV and wRBC comparably prevent VT/VF possible by attenuating ischemia-reperfusion injury in HS. Especially, even low concentration of hemoglobin in LHb is comparably effective with closely normal concentration of HbV.

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