by lylelinBuku Pengajian Malaysia Pdf 25 ((INSTALL)) ⬜
Buku Pengajian Malaysia Pdf 25
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Category:Malaysian magazines
Category:Education magazines
Category:Education in Malaysia
Category:Publications established in 1973
Category:1973 establishments in Malaysia
Category:Malay-language magazines
Category:Magazines established in 1973This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Neutrophil extracellular traps (NETs) are decoys of extracellular DNA, known to be a pro-inflammatory component, and are produced by neutrophils to trap and kill pathogenic bacteria. NETs formation is promoted by inflammatory stimuli such as lipopolysaccharide (LPS) and phorbol myristate acetate (PMA). Recently, NETs formation has also been implicated in the pathogenesis of metabolic diseases, such as type 2 diabetes and atherosclerosis. No information on NETs in T2DM or atherosclerosis is available, because assays to detect NETs in these pathologies are not optimized. Once NETs are induced in the presence of pathogenic bacteria, NETs are proposed to defend the host by entrapping bacteria. However, it is also postulated that once NETs are released from dying neutrophils, they could be bioactive mediators promoting tissue damage. A well-known example is myocardial ischemia/reperfusion, a condition commonly associated with organ transplantation, where NETs have been shown to be involved in the pathophysiology of ischemia/reperfusion injury. There are no data on NETs in vascular and cardiac diseases, and no assay to characterize NETs in these pathologies is available. Our preliminary data has demonstrated that NETs form in the presence of LPS in human monocyte-derived macrophages (MDM), human peripheral blood neutrophils, and cardiac myocytes. Upon LPS stimulation, monocytes release NETs within one hour, which then arrest and kill Escherichia coli and Listeria monocytogenes. We have optimized a NETs assay to detect NETs in these pathologies. The aims of this study are as follows. (1) To determine the role of NETs in
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