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Cooperative effects of inflammatory ...
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Chen, Chong.
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Cooperative effects of inflammatory mediators on leukocyte and cancer cell interactions with vascular endothelium.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Cooperative effects of inflammatory mediators on leukocyte and cancer cell interactions with vascular endothelium./
作者:
Chen, Chong.
面頁冊數:
159 p.
附註:
Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.
Contained By:
Dissertation Abstracts International75-01B(E).
標題:
Engineering, Biomedical. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3595571
ISBN:
9781303414084
Cooperative effects of inflammatory mediators on leukocyte and cancer cell interactions with vascular endothelium.
Chen, Chong.
Cooperative effects of inflammatory mediators on leukocyte and cancer cell interactions with vascular endothelium.
- 159 p.
Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.
Thesis (Ph.D.)--Tulane University School of Science and Engineering, 2013.
Inflammation is a driving force behind various lethal pathological conditions, including atherosclerosis and cancer metastasis. Inflammatory mediators are keys that unlock the immune response via triggering interactions of leukocytes and vascular endothelial cells. Oxidized low density lipoprotein (OxLDL), lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-alpha), and histamine are all strong activators of the inflammatory response, and they can be simultaneously produced during various inflammatory disorders. This study focuses on investigating the cooperative effect of TNF-alpha and histamine, as well as OxLDL and histamine on monocyte-endothelium interactions. Furthermore, the roles of LPS-activated monocytes and histamine in interactions of breast cancer cells with vascular endothelium are also explored. The results suggest that: 1) TNF-alpha and histamine have a synergistic effect on monocyte-endothelium interactions; 2) histamine cooperatively works with OxLDL to induce monocyte recruitment on endothelial cells; 3) OxLDL treated macrophages and mast cells respectively release TNF-alpha and histamine, which in turn synergistically increase the capture of monocytes by endothelial cells; 4) LPS activated monocytes secret TNF-alpha to activate endothelial cells and assist in adhesion of carcinoma cells to activated vascular endothelium; 5) exposure of activated endothelial cells to histamine exaggerates the carcinoma cell arrest, especially in the presence of LPS activated monocytes. In summary, this study implies that an increased risk of atherogenesis may be among the population affected by allergy or asthma and having lipid rich diet that leads to the production of TNF-alpha and OxLDL in body. It also highlights that the mechanism by which Gram-negative bacterial infection increases a risk of breast cancer metastasis through the cardiovascular system, and shows the necessity to develop better approaches for preventing this infection after surgical resection or before histamine combined IL-2 immune therapy in order to reduce a risk of cancer metastasis.
ISBN: 9781303414084Subjects--Topical Terms:
1017684
Engineering, Biomedical.
Cooperative effects of inflammatory mediators on leukocyte and cancer cell interactions with vascular endothelium.
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Inflammation is a driving force behind various lethal pathological conditions, including atherosclerosis and cancer metastasis. Inflammatory mediators are keys that unlock the immune response via triggering interactions of leukocytes and vascular endothelial cells. Oxidized low density lipoprotein (OxLDL), lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-alpha), and histamine are all strong activators of the inflammatory response, and they can be simultaneously produced during various inflammatory disorders. This study focuses on investigating the cooperative effect of TNF-alpha and histamine, as well as OxLDL and histamine on monocyte-endothelium interactions. Furthermore, the roles of LPS-activated monocytes and histamine in interactions of breast cancer cells with vascular endothelium are also explored. The results suggest that: 1) TNF-alpha and histamine have a synergistic effect on monocyte-endothelium interactions; 2) histamine cooperatively works with OxLDL to induce monocyte recruitment on endothelial cells; 3) OxLDL treated macrophages and mast cells respectively release TNF-alpha and histamine, which in turn synergistically increase the capture of monocytes by endothelial cells; 4) LPS activated monocytes secret TNF-alpha to activate endothelial cells and assist in adhesion of carcinoma cells to activated vascular endothelium; 5) exposure of activated endothelial cells to histamine exaggerates the carcinoma cell arrest, especially in the presence of LPS activated monocytes. In summary, this study implies that an increased risk of atherogenesis may be among the population affected by allergy or asthma and having lipid rich diet that leads to the production of TNF-alpha and OxLDL in body. It also highlights that the mechanism by which Gram-negative bacterial infection increases a risk of breast cancer metastasis through the cardiovascular system, and shows the necessity to develop better approaches for preventing this infection after surgical resection or before histamine combined IL-2 immune therapy in order to reduce a risk of cancer metastasis.
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