Incorporation of branched-chain fatty acid into cellular lipids and caspase-independent apoptosis in human breast cancer cell line, SKBR-3

Objective: The objective of this survey was to study the association between Helicobacter pylori infection and the severity of coronary atherosclerosis. Methods: The study population consisted of 961 consecutive patients (711 males and 250 females) who underwent coronary angiography for suspected or known coronary atherosclerosis. The patients' body mass index, blood pressure, the blood lipid, blood glucose, leukocyte count (109/L), neutrophil count (109/L), and Helicobacter pylori-specific IgG antibodies were performed. Coronary angiograms were scored according to vessel score and Gensini's score. Results: A significant association between H. pylori infection and coronary atherosclerosis as well as its severity was not find in this cross section study (p = 0.858). And, the level distribution of vessel score (p = 0.906) and Gensini's score (p = 0.905) were similar in the seropositivity group and seronegativity group of Helicobacter pylori infection. However, the level of fasting high-density lipoprotein cholesterol (mmol/L) (p = 0.013) was significantly lower in the seropositivity group than that in the seronegativity group of Helicobacter pylori infection. Conclusions: In conclusion, in the present study, a significantly correlation between Helicobacter pylori seropositivity and angiographically evaluated severity of atherosclerosis was not find. And, the present study showed a good correlation between Helicobacter pylori infection and decreased HDL cholesterol. However, the exact mechanisms need further study. Introduction Cardiovascular diseases, including coronary atherosclerosis remain the leading cause of deaths in the developed and developing countries despite of declining mortality. Understanding the etiology and pathophysiology of coronary atherosclerosis is essential in treating the disease and Published: 23 December 2009 Lipids in Health and Disease 2009, 8:59 doi:10.1186/1476-511X-8-59 Received: 1 November 2009 Accepted: 23 December 2009 This article is available from: http://www.lipidworld.com/content/8/1/59 © 2009 Jia et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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