1.Study on the dose-effect relationship of left carnitine on cardiomyocyte function protection in children with viral myocarditis
Jing HUANG ; Yuanyuan WU ; Tianhe XIA ; Xuxiang HE
Chinese Journal of Biochemical Pharmaceutics 2017;37(5):332-334
Objective To observe the protective effect of different doses of left carnitine on cardiomyocyte function in children with viral myocarditis.Methods94 cases of children with viral myocarditis were selected and divided into observation group and control group according to the random number table, 47 cases in each group.Both groups were treated with fructose 1,6-diphosphate(100~250mg/kg, add 150mL of 10% glucose in intravenous infusion, 1times/d) combined with left carnitine.Large dose group of left carnitine 100 mg/kg, low dose group 50mg/kg, all added 150mL of 5% glucose intravenous infusion, 1 times/d.The total effective rate, creatine kinase(CK), creatine kinase isoenzyme (CK-MB),lactate dehydrogenase (LDH), cardiac ejection fraction(EF), ventricular short axis shortening (FS) And the total incidence of adverse reactions were compared between two groups.ResultsThe total effective rates of two group were 93.62% and 87.23%.The level of CK,CK-MB,LDH in two groups were significantly decreased after treatment of two weeks(P<0.05), EF, FS were increased after treatment of two weeks(P<0.05).There was no significant difference in CK, CK-MB, LDH, EF and FS between the high dose group and the low dose group after treatment of two weeks.The overall incidence of adverse reactions in the high dose group was 25.53%, which was lower than that in the low dose group (8.51%,P<0.05).ConclusionThe use of low-dose left carnitine in children with viral myocarditis can effectively remove free radicals, protect cardiomyocyte function and improve myocardial energy metabolism and cardiac function, and safer than high-dose groups.
2.Progress in the construction and screening of random mutation library.
Jue CHEN ; Jiamin HUANG ; Tianhe YAN ; Xiaoyu PENG ; Jun LIN
Chinese Journal of Biotechnology 2021;37(1):163-177
Directed evolution is a cyclic process that alternates between constructing different genes and screening functional gene variants. It has been widely used in optimization and analysis of DNA sequence, gene function and protein structure. It includes random gene libraries construction, gene expression in suitable hosts and mutant libraries screening. The key to construct gene library is the storage capacity and mutation diversity, to screen is high sensitivity and high throughput. This review discusses the latest advances in directed evolution. These new technologies greatly accelerate and simplify the traditional directional evolution process and promote the development of directed evolution.
Base Sequence
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Directed Molecular Evolution
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Gene Library
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Mutation
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Proteins/genetics*
3.AAZ2 induces mitochondrial-dependent apoptosis by targeting PDK1 in gastric cancer.
Yi LI ; Wenyan SHE ; Xiaoran XU ; Yixin LIU ; Xinyu WANG ; Sheng TIAN ; Shiyi LI ; Miao WANG ; Chaochao YU ; Pan LIU ; Tianhe HUANG ; Yongchang WEI
Journal of Zhejiang University. Science. B 2023;24(3):232-247
Drastic surges in intracellular reactive oxygen species (ROS) induce cell apoptosis, while most chemotherapy drugs lead to the accumulation of ROS. Here, we constructed an organic compound, arsenical N-(4-(1,3,2-dithiarsinan-2-yl)phenyl)acrylamide (AAZ2), which could prompt the ROS to trigger mitochondrial-dependent apoptosis in gastric cancer (GC). Mechanistically, by targeting pyruvate dehydrogenase kinase 1 (PDK1), AAZ2 caused metabolism alteration and the imbalance of redox homeostasis, followed by the inhibition of phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway and leading to the activation of B-cell lymphoma 2 (Bcl2)/Bcl2-associated X (Bax)/caspase-9 (Cas9)/Cas3 cascades. Importantly, our in vivo data demonstrated that AAZ2 could inhibit the growth of GC xenograft. Overall, our data suggested that AAZ2 could contribute to metabolic abnormalities, leading to mitochondrial-dependent apoptosis by targeting PDK1 in GC.
Humans
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Signal Transduction
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Stomach Neoplasms/drug therapy*
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Reactive Oxygen Species/metabolism*
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Proto-Oncogene Proteins c-akt/metabolism*
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Apoptosis
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Proto-Oncogene Proteins c-bcl-2
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Cell Line, Tumor