Background & Aim: PNETs are rare and usually require surgical excision.Our aim was to evaluate whether EUS-FNA influenced the surgical decision-making when compared to other imaging modalities.Methods: Our surgical, histologic, and endoscopic databases were reviewed between 2/2000 -11/2009 to identify all patients with histologically proven PNETs.Demographics, symptoms, imaging studies, treatment decisions, and operative reports were reviewed.EUS findings were compared to CT, MRI, and nuclear scan findings.Results: Forty-seven patients (mean age 63 yrs, [range 28-83], 20 male) underwent EUS-FNA of pancreatic lesions that proved to be PNETs.The most common indications for EUS were discovery of tumors on CT or MRI (n=38) or presence of symptoms (n=9).Mean tumor size on EUS was 22.9 mm (5.9-50 mm).Seven tumors were located in the uncinate process, 13 in the head, 17 in the body, and 16 in the tail.Twenty-nine patients underwent surgery (9 whipples, 18 distals, 1 partial head resection, 1 enucleation), while 3 more are awaiting surgery.Of 46 CT scans, 17 MRIs, and 12 nuclear scans (PET/octreoscan), tumor was not seen in 10, 3, and 7 studies, respectively.In 9 patients (19%) who were shown to have a PNET by EUS-FNA, no other imaging technique showed tumor presence.Of these 9 patients, 5 had surgery, 1 elected to delay surgery, and 3 did not have surgery due to metastatic disease on EUS-FNA.Another patient underwent surgery after EUS excluded peripancreatic metastasis that was suggested on CT, and 1 patient did not have surgery after EUS showed vascular invasion that was not detected by CT.There were no cases of tumors evident on CT/MRI that were missed on EUS.Conclusion: EUS-FNA is more sensitive and specific than CT or MRI in detecting PNETs.It changed the surgical management in 11/47 (23%) patients by detecting tumors undetected by other imaging modalities in 9 patients, excluding metastatic disease in 1 patient, and showing vascular invasion by tumor in another one.Our data suggest, therefore, that EUS is more cost effective than CT/MRI and should be used as the main imaging test for the management of suspected PNETs.

Background: Nitric oxide is an endothelium dependent dilator, which may protect against atherosclerosis. Several Studies have shown a decrease in nitric oxide activity with aging, however none have assessed aging and atherosclerosis separately. We tested the hypothesis that aging blunts both basal and receptor-mediated endothelial nitric oxide release in humans.Methods: We examined whether forearm blood flow responses to intra-arterial acetylcholine, and nitroprusside, were altered with aging with and without co-infusion of an inhibitor of nitric oxide synthase (N-G-mono-methyl-L-arginine) in three groups Of human subjects a group with clinical atherosclerotic vascular disease (n = 31, 21 M), otherwise healthy elderly (n = 17, 13 M), and healthy young Controls (n = 15 8 M).Results: There was no difference in basal flows between the three groups. There was also no difference in the dilatation to either acetylcholine or nitroprusside responses between the AVD and the healthy elderly group; however, aging significantly decreased acetylcholine or nitroprusside responses when compared to the Young controls (p < 0.02). Furthermore, the ratio between acetylcholine and nitroprusside. a marker of endothelial NO synthase activity, was significantly greater in the young Volunteers (0.816 +/- 0.094% vs. 0.892 +/- 0.146 % vs. 1.389 +/- 0.2%. in atherosclerotic vascular disease, healthy elderly group, and young controls respectively).Conclusions: Forearm blood flow responses to endothelium dependent and independent Stimuli are blunted with aging, independent of the presence of atherosclerotic disease. Moreover, the normal aging process may induce significant global vascular dysfunction (involving the endothelium and the vascular smooth muscle), to as great a degree as clinically manifest atherosclerosis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Elevated low-density lipoprotein (LDL)-cholesterol is associated with a significantly increased risk of coronary heart disease. Ezetimibe is the first member of a new class of selective cholesterol absorption inhibitors. It impairs the intestinal reabsorption of both dietary and hepatically excreted biliary cholesterol. Ezetimibe is an effective and safe agent for lowering LDL-C and non HDL-C. Short term clinical trials have established the role of ezetimibe monotherapy and its use in combination with statins. Furthermore, ezetimibe and statin combination therapy increased the percentage of patients who achieved their LDL-C treatment goal. Studies using surrogate markers of atherosclerosis have suggested a possible role of ezetimibe in combating atherosclerosis. Ezetimibe provides an effective therapeutic strategy for the management of homozygous familial hypercholesterolemia (HoFH) and sitosterolemia. The lack of outcomes and long term safety data is attributed to the relatively recent introduction of this medication. Background Over 60 million Americans suffer from cardiovascular disease (CHD). The incidence of CHD and stroke has been on the rise partly because of the increase in life expectancy and the explosive epidemic of diabetes and the metabolic syndrome [1]. CHD is responsible for about 38% of the overall mortality in the United States making it the number one killer of Americans [2]. Animal and human studies have established the role of cholesterol in the development and progression of atherosclerosis. LDL-cholesterol (LDL-C) constitutes approximately 60–70 % of total serum cholesterol. Epidemiological studies directly implicated LDL-C to the development of atherosclerosis and CHD. Furthermore, LDL-C level appears to be directly related to the development and recurrence of CHD [3]. Animal studies suggested a protective effect of low LDL-C against atherosclerosis [2]. Multiple human trials examining the relationship of LDL-C lowering in primary and secondary prevention of CHD have demonstrated the impact of reducing LDL-C levels on decreasing CHD and CHD related mortality [4-8]. Published: 07 October 2004 Lipids in Health and Disease 2004, 3:22 doi:10.1186/1476-511X-3-22 Received: 23 September 2004 Accepted: 07 October 2004 This article is available from: http://www.lipidworld.com/content/3/1/22 © 2004 Al-Shaer 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.

Elevated low-density lipoprotein (LDL)-cholesterol is associated with a significantly increased risk of coronary heart disease. Ezetimibe is the first member of a new class of selective cholesterol absorption inhibitors. It impairs the intestinal reabsorption of both dietary and hepatically excreted biliary cholesterol. Ezetimibe is an effective and safe agent for lowering LDL-C and non HDL-C. Short term clinical trials have established the role of ezetimibe monotherapy and its use in combination with statins. Furthermore, ezetimibe and statin combination therapy increased the percentage of patients who achieved their LDL-C treatment goal. Studies using surrogate markers of atherosclerosis have suggested a possible role of ezetimibe in combating atherosclerosis. Ezetimibe provides an effective therapeutic strategy for the management of homozygous familial hypercholesterolemia (HoFH) and sitosterolemia. The lack of outcomes and long term safety data is attributed to the relatively recent introduction of this medication.