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Infection-stimulated Anemia Results Primarily from Interferon Gamma-dependent, Signal Transducer and Activator of Transcription 1-independent Red Cell Loss 被引量:1
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作者 Zheng Wang dong-xia zhang Qi Zhao 《Chinese Medical Journal》 SCIE CAS CSCD 2015年第7期948-955,共8页
Background: Although the onset of anemia during infectious disease is commonly correlated with production of inflammatory cytokines, the mechanisms by which cytokines induce anemia are poorly defined. This study focu... Background: Although the onset of anemia during infectious disease is commonly correlated with production of inflammatory cytokines, the mechanisms by which cytokines induce anemia are poorly defined. This study focused on the mechanism research. Methods: Different types of mice were infected perorally with Toxoplasma gondii strain ME49. At the indicated times, samples fi'om each mouse were harvested, processed, and analyzed individually. Blood samples were analyzed using a Coulter Counter and red blood cell (RBC) survival was measured by biotinylation. Levels of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), and inducible protein 10 (IP-10) mRNA in liver tissue were measured by real-time polymerase chain reaction. Results: T. gondii-infected mice exhibited anemia due to a decrease in both erythropoiesis and survival time of RBC in the circulation (P 〈 0.02). In addition, infection-stimulated anemia was associated with fecal occult, supporting previous literature that hemorrhage is a consequence of T. gondii infection in mice. Infection-induced anemia was abolished in interferon gamma (IFNy) and I FNy receptor deficient mice (P 〈 0.05) but was still evident in mice lacking TNF-α, iNOS, phagocyte NADPH oxidase or IP-10 (P 〈 0.02). Neither signal transducer and activator of transcription 1 (STAT1) deficient mice nor 129S6 controls exhibited decreased erythropoiesis, but rather suffered from an anemia resulting solely from increased loss of circulating RBC. Conclusions: Infection-stimulated decrease in erythropoiesis and losses of RBC have distinct mechanistic bases. These results show that during T. gondii infection, IFNγ is responsible foran anemia that results from both a decrease in erythropoiesis and a STAT1 independent loss of circulating RBC. 展开更多
关键词 ANEMIA Helnorrhage Signal Transducer and Activator of Transcription 1 Tmot)lasma gondii
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Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit Ⅱ 被引量:1
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作者 Fei Xiang Si-yuan Ma +3 位作者 Yan-ling Lv dong-xia zhang Hua-pei Song Yue-sheng Huang 《Burns & Trauma》 SCIE 2019年第1期139-149,共11页
Background:Tumor necrosis factor receptor-associated protein 1(TRAP1)plays a protective effect in hypoxic cardiomyocytes,but the precise mechanisms are not well clarified.The study is aimed to identify the mechanism o... Background:Tumor necrosis factor receptor-associated protein 1(TRAP1)plays a protective effect in hypoxic cardiomyocytes,but the precise mechanisms are not well clarified.The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes.Methods:In this study,the effects of TRAP1 and cytochrome c oxidase subunit Ⅱ(COXⅡ)on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods separately.Results:Hypoxia induced cardiomyocyte apoptosis,and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia.Conversely,TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes.Further investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXⅡ overexpression,whereas COXⅡ knockdown reduced the antiapoptotic function induced by TRAP1 overexpression.Additionally,changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm,as well as reactive oxygen species production,were found to be correlated with the changes in apoptosis.Conclusions:The current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXⅡ,in which reactive oxygen species presents as an important component. 展开更多
关键词 CARDIOMYOCYTES HYPOXIA Tumor necrosis factor receptor-associated protein 1 Cytochrome c oxidase subunitⅡ Reactive oxygen species APOPTOSIS
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Preparation of chitosan/N-doped graphene natively grown on hierarchical porous carbon nanocomposite as a sensor platform for determination of tartrazine
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作者 Zhen-Zhen An Zhuang Li +6 位作者 Yong-Yang Guo Xiao-Ling Chen Kang-Ning zhang dong-xia zhang Zhong-Hua Xue Xi-Bin Zhou Xiao-Quan Lu 《Chinese Chemical Letters》 SCIE CAS CSCD 2017年第7期1492-1498,共7页
In this work,the chitosan and N-doped graphene natively grown on hierarchical porous carbon(N-PC-G/CS) nanocomposite was obtained by ultrasonic method,as a novel sensor platform for determination of tartrazine(TT)... In this work,the chitosan and N-doped graphene natively grown on hierarchical porous carbon(N-PC-G/CS) nanocomposite was obtained by ultrasonic method,as a novel sensor platform for determination of tartrazine(TT).The nanocomposite as prepared had well dispersivity in water and excellent conductivity.The N-PC-G/CS nanocomposite was characterized by scanning electron microscopy(SEM),transmission electron microscopy(TEM),nitrogen adsorption-desorption,fourier transform infrared(FTIR) and electrochemical impedance spectroscopy(EIS).The application of N-PC-G/CS for determination of tartrazine(TT) was investigated by chronocoulometry(CC),cyclic voltammetry(CV) and differential pulse voltammetry(DPV).Under optimized conditions,the sensor displayed a sensitive response to TT within a wide concentration range of 0.05-15.0 μmol/L,the detection limits is 0.036 μmol/L(S/N = 3).Furthermore,this nanocomposite could be efficiently applied for determination of TT in soft drink samples. 展开更多
关键词 Porous carbon Graphene Chitosan Sensor Tartrazine
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