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774 results on '"Gao, Xiao-Ming"'

205. Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia–reperfusion injury: A predominant role of anti-inflammation

Author

Gao, Xiao-Ming, primary, Liu, Yang, additional, White, David, additional, Su, Yidan, additional, Drew, Brian G., additional, Bruce, Clinton R., additional, Kiriazis, Helen, additional, Xu, Qi, additional, Jennings, Nicole, additional, Bobik, Alex, additional, Febbraio, Mark A., additional, Kingwell, Bronwyn A., additional, Bucala, Richard, additional, Fingerle-Rowson, Günter, additional, Dart, Anthony M., additional, Morand, Eric F., additional, and Du, Xiao-Jun, additional

Published
2011
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207. Novel Role of Platelets in Mediating Inflammatory Responses and Ventricular Rupture or Remodeling Following Myocardial Infarction

Author

Liu, Yang, primary, Gao, Xiao-Ming, additional, Fang, Lu, additional, Jennings, Nicole L., additional, Su, Yidan, additional, Q, Xu, additional, Samson, Andre L., additional, Kiriazis, Helen, additional, Wang, Xin-Feng, additional, Shan, Leonard, additional, Sturgeon, Sharelle A., additional, Medcalf, Robert L., additional, Jackson, Shaun P., additional, Dart, Anthony M., additional, and Du, Xiao-Jun, additional

Published
2011
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213. PI3K(p110α) Protects Against Myocardial Infarction-Induced Heart Failure

Author

Lin, Ruby C.Y., primary, Weeks, Kate L., additional, Gao, Xiao-Ming, additional, Williams, Rohan B.H., additional, Bernardo, Bianca C., additional, Kiriazis, Helen, additional, Matthews, Vance B., additional, Woodcock, Elizabeth A., additional, Bouwman, Russell D., additional, Mollica, Janelle P., additional, Speirs, Helen J., additional, Dawes, Ian W., additional, Daly, Roger J., additional, Shioi, Tetsuo, additional, Izumo, Seigo, additional, Febbraio, Mark A., additional, Du, Xiao-Jun, additional, and McMullen, Julie R., additional

Published
2010
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232. Targeting transgene to the heart and liver with AAV9 by different promoters.

Author

Chen, Bang‐Dang, He, Chun‐Hui, Chen, Xiao‐Cui, Pan, Shuo, Liu, Fen, Ma, Xiang, Li, Xiao‐Mei, Gai, Min‐Tao, Tao, Jing, Ma, Yi‐Tong, Yang, Yi‐Ning, and Gao, Xiao‐Ming

Subjects
CARDIOPULMONARY system, TRANSGENE expression, SMALL molecules, DRUG therapy, BIOTECHNOLOGY, PHARMACOLOGY
Abstract

Adeno-associated virus ( AAV) has become one of the most promising gene transfer tools for gene therapy. This work aims to evaluate tropism, gene transfer efficiency and safety of AAV9 vectors produced with recombinant baculovirus ( rBac)-based system. AAV9- CMV- GFP and AAV9- CBA- GFP were produced using a rBac system, 1 × 1011 particles of each vectors were administered intravenously (i.v.) into mice and animals were killed at 1, 2, 3, 4, 5 and 8 weeks after administration. The GFP expression in different organs was analyzed by fluorescence imaging and Western blot. Viral genomic quantities were measured using qPCR. In vitro transduction efficiency of AAV9 vectors in primary cardiomyocytes and hepatocytes was determined by flow cytometry. Toxicity of AAV9 vectors was evaluated by determining certain cardiac and liver injury biomarkers and renal function test in vivo and TUNEL analysis in vitro. The data showed that AAV9 viral particles packaged by the rBac system were fully functional in vivo and in vitro. The CMV promoter predominantly induced higher cardiac GFP transgene expression and DNA copy numbers while the CBA promoter resulted in robust GFP expression and high vector DNA copy numbers in mouse liver, both in a time-dependent increased manner. Such distinct preferential effects were also observed in the heart and liver as early as 3 and 5 days after co-infection. Both the AAV9- CMV and AAV9- CBA viral packages did not induce heart, liver and renal damage and cell apoptosis. These results indicated that AAV9- CMV can efficiently and safely direct cardiac gene transfer, whereas AAV9- CBA is preferential for liver gene delivery. [ABSTRACT FROM AUTHOR]

Published
2015
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233. Pathological hypertrophy reverses β2-adrenergic receptor-induced angiogenesis in mouse heart.

Author

Xu, Qi, Jennings, Nicole L., Sim, Kenneth, Chang, Lisa, Gao, Xiao‐Ming, Kiriazis, Helen, Lee, Ying Ying, Nguyen, My‐Nhan, Woodcock, Elizabeth A., Zhang, You‐Yi, El‐Osta, Assam, Dart, Anthony M., and Du, Xiao‐Jun

Subjects
HYPERTROPHY, ADRENERGIC receptors, NEOVASCULARIZATION, VASCULAR endothelial cells, PHOSPHORYLATION, VASCULAR endothelial growth factors
Abstract

β-adrenergic activation and angiogenesis are pivotal for myocardial function but the link between both events remains unclear. The aim of this study was to explore the cardiac angiogenesis profile in a mouse model with cardiomyocyte-restricted overexpression of β2-adrenoceptors ( β2- TG), and the effect of cardiac pressure overload. β2- TG mice had heightened cardiac angiogenesis, which was essential for maintenance of the hypercontractile phenotype seen in this model. Relative to controls, cardiomyocytes of β2- TGs showed upregulated expression of vascular endothelial growth factor ( VEGF), heightened phosphorylation of cAMP-responsive-element-binding protein ( CREB), and increased recruitment of phospho- CREB, CREB-binding protein ( CBP), and p300 to the VEGF promoter. However, when hearts were subjected to pressure overload by transverse aortic constriction ( TAC), angiogenic signaling in β2- TGs was inhibited within 1 week after TAC. β2- TG hearts, but not controls, exposed to pressure overload for 1-2 weeks showed significant increases from baseline in phosphorylation of Ca2+/calmodulin-dependent kinase II (Ca MKIIδ) and protein expression of p53, reduction in CREB phosphorylation, and reduced abundance of phospho- CREB, p300 and CBP recruited to the CREB-responsive element ( CRE) site of VEGF promoter. These changes were associated with reduction in both VEGF expression and capillary density. While non- TG mice with TAC developed compensatory hypertrophy, (2- TGs exhibited exaggerated hypertrophic growth at week-1 post- TAC, followed by LV dilatation and reduced fractional shortening measured by serial echocardiography. In conclusion, angiogenesis was enhanced by the cardiomyocyte (2 AR/ CREB/ VEGF signaling pathway. Pressure overload rapidly inhibited this signaling, likely as a consequence of activated Ca MKII and p53, leading to impaired angiogenesis and functional decompensation. [ABSTRACT FROM AUTHOR]

Published
2015
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234. Medical logic module (MLM) representation of knowledge in a ventilator treatment advisory system

Author

Ludwigs Ulf, Shahsavar Nosrat, Gao Xiao-ming, Arkad Kristina, Gill Hans, and Wigertz Ove

Subjects
Decision support system, Knowledge representation and reasoning, business.industry, Ventilator treatment, fungi, Representation (systemics), Medicine (miscellaneous), computer.file_format, Assisted ventilation, Critical Care and Intensive Care Medicine, humanities, Arden syntax, Advisory system, stomatognathic system, Logic module, Artificial Intelligence, Therapy, Computer-Assisted, Acute Disease, Humans, Medicine, Artificial intelligence, Respiratory Insufficiency, business, Software engineering, computer
Abstract

In any medical expert system it is the inherent knowledge that is the power of the system and not the particulars of its implementation. Therefore it would be valuable to use a representation that would allow: knowledge transfer between different systems, users, experts and 'importers' to be able to evaluate the logic, experts to easily input their knowledge and be guided how to use the syntax. Adren Syntax of Medical Logic Module is a proposed knowledge representation, fulfilling these criteria. The Arden Syntax has been used to represent rules and logic in a decision support system for ventilator therapy in patients with acute respiratory failure (ARF) that is under development. The medical experts involved in the project have used the Arden Syntax as a convenient way for transfer and storage of medical knowledge. The syntax is easy to learn and may be used with a minimum of training. In the present system, Medical Logical Modules have been used to represent knowledge pertinent to the initiation and maintenance phases of ventilator therapy.

Published
1991

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