Additionally, the results suggest that transposition and Folic acid homologous recombination mediated by IS26 as well as transformation of cfr-carrying plasmids may be the main mechanism for horizontal spread of the cfr gene in E. coli. Further surveillance and investigation are necessary to facilitate the control of cfr spread in gram-negative bacteria. High salt intake has been associated with hypertension in some but not all human association studies. Randomized controlled trials suggest that modest reduction in salt intake over periods of 4�C52 weeks leads to significant lowering in blood pressure by 3�C4 mmHg. Meta-analyses of prospective studies also suggest that high salt intake is associated with greater risk of stroke. Current clinical guidelines and public health policies recommend low salt intake. There have been, however, reports of increased cardiovascular death associated with low salt intake and there is ongoing controversy over the most appropriate amount of salt intake. Population screening studies suggest that history of hypertension is a risk factor for abdominal aortic aneurysm, and several animal models utilize salt intake as part of an induction regimen to stimulate aneurysm formation within the aorta and at other arterial sites. A meta-analysis of large surveillance studies also suggests that hypertension increases the risk of AAA rupture. Based on these data, restricting salt intake should reduce the incidence of AAA, although no clinical studies have assessed the association of salt intake with AAA. The aim of this study was to assess the association of reported salt intake with AAA prevalence. In order to examine this aim we utilized data from the Health In Men Study. The main findings from this study were that sometimes or always adding salt to food was associated with increased prevalence of AAA and larger infrarenal aortic diameter in older men. The reliability of this association is supported by the large number of men examined, the demonstrated reproducible method of aortic imaging used, the adjustment for potential confounding risk factors, and the consistency of the association when men with previous cardiovascular disease or relevant risk factors were excluded. We believe this to be the first study to examine the association of reported salt intake with aortic aneurysm in humans. The role of high salt intake in aortic aneurysm formation has been previously Diperodon examined in three rodent model studies. Nishijo and colleagues examined the effect of adding 1% sodium chloride to the drinking water of transgenic mice that overproduced angiotensin II. They reported that mice receiving salt loading developed thoracic and abdominal aortic aneurysms which ruptured in 67% of animals during 30 days of salt administration. Nishijo et al. reported that salt loading stimulated an increase in drinking volume and plasma atrial natriuretic peptide associated with loss of aortic vascular smooth muscle cells. Kanematsu and colleagues administered the mineralocorticoid deoxycorticosterone acetate, 1% salt and a lysyl oxidase inhibitor, which blocks cross-linking of elastin and collagen, to male C57BL/6J mice. This regimen induced thoracic 
and abdominal aortic aneurysms associated with hypertension, aortic wall inflammation and disruption of elastic laminae. Finally, Liu and colleagues examined the effect of the administration of the mineralocorticoid receptor agonists deoxycorticosterone acetate and aldosterone in addition to 1% salt.