1.Isolation and identification of leukemia stem cells from acute myeloid leukemia patients
Weichun XIAO ; Jinzhi LU ; Tao LI ; Weijing CHEN ; Shengdong LU
Journal of Leukemia & Lymphoma 2010;19(9):523-525
Objective To isolate and identify leukemia stem cells from acute myeloid leukemia patients for further research. Methods By Ficoll density gradient centrifugation, mononuclear cells were firstly separated from bone marrow of patients. According to specific surface markers, CD+34 CD+123 of leukemic stem cells were sorted by flow cytometer. Their ability of self-renewal and differentiation were evaluated by colony formation and cobblestone forming ability. At the same time, the purity and cell morphology of CD+34 CD+123 cells was analysed. Results Comparared with total mononuclear cells, the proportion of the CD+34 CD+123 cells after sorting was 10.7 %, and these cells showed the ability of colony forming and cobblestone forming, and the purity proportion of CD+34 CD+123 cells was 62.1%. Conclusion The leukemia stem cells were isolated successfully and could be used in further study.
2.Role of mitochondrial injury in the development and progression of nonalcoholic fatty liver disease
Journal of Clinical Hepatology 2021;37(7):1515-1521.
Mitochondria are an important organelle and can regulate lipid metabolism, oxidative phosphorylation, and ATP synthesis. Disorder of mitochondria biosynthesis, loss of mitochondrial homeostasis, and even mitochondrial structural damage will lead to lipid metabolism disorders and oxidative stress. Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by lipid accumulation in hepatocytes. NAFLD is a progressive disease manifesting as the process from hepatocyte steatosis to steatohepatitis, liver fibrosis, and liver cirrhosis. It is currently believed that mitochondria play an important role in the onset of NAFLD, and thus NAFLD is also referred to as “mitochondrial disease”. This article reviews the association of mitochondrial injury, such as lipid metabolism disorders, change in reactive oxygen species, and loss of mitochondrial homeostasis, with the development and progression of NAFLD.