Background-This study evaluated a possible relationship between levels of endothelial microparticles (EMPs), known to be a sensitive indicator of endothelial disturbance, and changes in postprandial lipid levels in healthy volunteers after a low-or high-fat meal. Methods and Results-Eighteen healthy subjects without known cardiovascular risk factors were evaluated. Lipid and EMP levels were measured before and 1 and 3 hours after a single low-or high-fat isocaloric meal. The low-fat meal had no significant postprandial effect on EMPs or lipids compared with fasting levels. In contrast, a single high-fat meal significantly increased EMP levels after 1 and 3 hours, from 389Ϯ54 (thousands per milliliter) when fasting to 541Ϯ139 (Pϭ0.0002) and 677Ϯ159 (PϽ0.0001), respectively, and correlated with a postprandial elevation in serum triglycerides. Conclusions-A single high-fat meal led to a significant elevation of plasma EMP levels in healthy, normolipidemic subjects and correlated with a postprandial elevation of serum triglycerides. 4,5 Hypertriglyceridemia has been shown to be an independent risk factor for coronary artery disease, 6,7 and increasing evidence suggests that postprandial hyperlipidemia contributes to the development of atherosclerosis and coronary artery disease. 8 -11 Moreover, several studies have demonstrated that postprandial hypertriglyceridemia can impair endothelial function, suggesting a role for triglycerides in the initiation and progression of atherosclerosis. [12][13][14] In vitro activation or apoptosis of cultured ECs induces the release of endothelial microparticles (EMPs). 15 EMPs in plasma exhibit the same antigenic markers and are detected and counted by flow cytometry, providing information on the degree of endothelial injury 16 -18 and even on the nature of the damage. 15 High levels of EMPs were reported in patients with thrombotic thrombocytopenic purpura, 16 preeclampsia, 17 acute coronary syndromes, 18,21 malignant hypertension, 19 multiple sclerosis, 20 and atherosclerotic plaques, 22 implicating EMPs as a marker of endothelial damage.In this article, we demonstrate a direct correlation between endothelial disturbance, measured by plasma EMP levels, and postprandial changes in serum triglycerides in healthy individuals after a single high-fat meal. No changes in EMP levels or serum lipids were observed after an isocaloric low-fat meal. These results suggest a link between postprandial hyperlipidemia and injury of the blood vessel wall. Methods Study SubjectsWe enrolled a total of 18 (10 male, 8 female; mean age, 26Ϯ3.8 years) healthy normolipidemic volunteers randomly selected from the medical center house staff. Subjects were nonobese, with a mean body mass index of 23Ϯ2.3 kg/m 2 , and normoglycemic, with a mean insulin level of 10Ϯ14 IU/mL. Subjects with dyslipidemia were excluded. The study protocol was approved and performed under the guidelines of our Institutional Review Board. Informed consent was obtained from each individual. Diet ProtocolThe diet protocol cons...

We report a case of subacute bacterial endocarditis associated with small vessel vasculitis and a strongly positive cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) test. It is important to recognize this cause of positive c-ANCA because infectious endocarditis may closely mimic the clinical manifestations of ANCA-associated vasculitides such as Wegener granulomatosis or microscopic polyangiitis. Furthermore, ANCA-associated vasculitis may result in noninfectious endocarditis, which may be confused with bacterial endocarditis. In this paper, we review reported cases of ANCA-positive bacterial endocarditis and compare them to the reported cases of ANCA-associated idiopathic vasculitis with endocardial compromise.

Function and survival of cells depend in part on the presence of growth factors. We explored the autocrine regulation of insulin and nerve growth factor (NGF) on single adult rat pancreatic ␤-cell survival and hormone secretion. When NGF or insulin signaling were blocked in culture media, cell survival decreased compared with control cells, with apoptosis being the main mechanism of cell death. To further explore the role of glucose in ␤-cell survival, we cultured the cells for 16 h in 2.6 mmol/l glucose and observed that nearly 17% of the cells developed apoptosis; this effect was partially prevented by NGF and almost completely inhibited by insulin treatment. A high K ؉ concentration had the same effect, suggesting that insulin and NGF secretion by the cells was responsible for the survival effects and not glucose per se. Blocking NGF signaling with an NGF antibody or with K252a reduced insulin biosynthesis and secretion in the cells that survived the treatment. Moreover, the functional ␤-cell subpopulation with a higher insulin secretion rate is more susceptible to K252a. These results further indicate that NGF and insulin play important autoregulatory roles in pancreatic ␤-cell survival and function and strongly suggest the need to explore new focuses in diabetes treatment.

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