Phthalate esters are used widely as plasticizers for polyvinylchloride (PVC) formulations in several applications, including medical devices, toys, food wraps, and building products, to impart flexibility to an otherwise rigid PVC. Di-(2-ethylhexyl)phthalate (DEHP) is the most commonly used plasticizer. Because DEHP does not bind with the plastic, it leaches with time and use from vinyl products, thus becoming a ubiquitous environmental contaminant (Bauer and Herrmann 1997;Bradbury 1996;Giam et al. 1978;Griffiths et al. 1985;Mayer et al. 1972;Mes et al. 1974;Øie et al. 1997;Sharman et al. 1994). In particular, leaching of DEHP from PVC medical devices and deposits in tissue have been well documented (Latini 2000;Tickner et al. 2001). Because the DEHP action depends on dose, time, and age (Latini 2000) and because DEHP effects are influenced by the stage of development at exposure among animals (Akingbemi et al. 2001), the DEHP-related exposure risk is potentially higher for the developing fetus and newborn, particularly preterm. Recently, our preliminary findings indicated that the exposure to these environmental contaminants begins during intrauterine life, that these chemicals are able to cross the placental barrier, and that fetal exposure is closely related to maternal exposure (Latini et al. 2003). The aim of this study was to measure concentrations of DEHP and/or its main metabolite, mono-(2-ethylhexyl)phthalate (MEHP), in a larger population of human neonates and to evaluate possible biologic effects from prenatal exposure to DEHP and/or MEHP. Patients and MethodsSubjects. Cord blood samples were collected from 84 consecutive newborns (82 singletons, two twins), born at the general-practice Brindisi Hospital, with the following characteristics: 39 male, 45 female; maternal age at delivery, 29.5 ± 5.1 years (range = 18-42); vaginal delivery, n = 65 (77.4%); gestational age, 38.4 ± 2.2 weeks (range = 27-42); birth weight, 3,220 ± 680 g, (range = 1,150-4,350); 1-min Apgar score, 7.9 ± 0.9; 5-min Apgar score, 8.8 ± 0.5. Eleven of 84 infants were preterm; only three had very low birth weight. Moreover, four infants who were small for gestational age (SGA) were present in our population. None of the examined infants was born after in vitro fertilization pregnancy. The study was approved by the ethics committee of the Brindisi Hospital (Brindisi, Italy), and written informed consent from the parents was obtained. Blood specimens were immediately centrifuged (3,500 × g, 7 min), and serum was stored at -20°C until assay. To avoid any contamination from plasticizers in lab equipment, the serum sample collection, preservation, and treatment were performed only with glass devices. The concentrations of DEHP and MEHP were determined by highperformance liquid chromatography, at the Department of Chemistry of the University of L'Aquila, an institution certified in agreement with the International Organization for Standardization 9001 quality system, as described previously .Data analysis. Data are expressed as mean ± SD...

The present findings showed for the first time an association between DEHP plasma concentrations and endometriosis, suggesting a possible role for phthalate esters in the pathogenesis.

Ordered arrays of light-emitting conjugated polymer nanofibers are realized by near-field electrospinning.

Background: Di(2-ethylhexyl)phthalate (DEHP), the most commonly used plasticizer, is a widespread ubiquitous environmental contaminant. The potential health hazards from exposure to DEHP and its main metabolite, mono(2-ethylhexyl)phthalate (MEHP), have been well documented. Exposure to DEHP and MEHP in humans at risk, such as pregnant women and human fetuses, has not been tested. Methods: Plasma DEHP and MEHP concentrations were measured in a total of 24 consecutive mother-infant pairs by high performance liquid chromatography. Associations between DEHP/MEHP and infant characteristics were tested using Fisher’s exact test, unpaired t tests and univariate linear regression analysis. Results: Measurable DEHP and MEHP concentrations were found in 17/24 (70.8%) and 18/24 (75%) maternal plasmas, respectively, and in 11/25 (44%) and 18/25 (72.0%) cord samples, respectively. Either DEHP or MEHP were detectable in 21/24 (87.5%) maternal plasmas and 19/25 (76%) cord samples. The mean DEHP concentrations in maternal and cord plasmas were 1.15 ± 0.81 and 2.05 ± 1.47 µg/ml, respectively. The mean MEHP concentrations were 0.68 ± 0.85 and 0.68 ± 1.03 µg/ml, respectively. No significant correlations were found between maternal and cord blood DEHP, maternal and cord blood MEHP, maternal DEHP and cord blood MEHP, or maternal MEHP and cord blood DEHP plasma concentrations. Conclusion: Although the effects of perinatal exposure to phthalates need further research, our findings: (i) confirm the high frequency of DEHP and/or MEHP exposure in human pregnancies; (ii) indicate that the exposure to these environmental contaminants begins during intrauterine life, and (iii) suggest that fetal exposure is closely related to the maternal exposure.

Abstract-Nitric oxide plays a pivotal role in regulating vascular tone. Different studies show endothelial function is impaired during hyperglycemia. Dark chocolate increases flow-mediated dilation in healthy and hypertensive subjects with and without glucose intolerance; however, the effect of pretreatment with dark chocolate on endothelial function and other vascular responses to hyperglycemia has not been examined. Therefore, we aimed to investigate the effects of flavanol-rich dark chocolate administration on (1) flow-mediated dilation and wave reflections; (2) blood pressure, endothelin-1 and oxidative stress, before and after oral glucose tolerance test (OGTT 1 Atherosclerotic pathology is a common sequela to T2DM, with macrovascular and microvascular diseases being among the leading causes of morbidity and mortality in patients with T2DM.2 Even after adjustment for conventional risk factors, individuals with T2DM exhibit a 2-to 4-fold increased risk of mortality in comparison with individuals without diabetes.3 Thus, several investigations have been directed to the potential adverse effects of hyperglycemia on the arterial wall. Observational data reveal high blood glucose concentrations are a risk factor for mortality, even in nondiabetic individuals. 4 Postprandial hyperglycemia has also been implicated in the development of cardiovascular disease. Elevated postprandial glucose may have a direct toxic effect on the vascular endothelium mediated by oxidative stress, independent of other cardiovascular risk factors, such as hyperlipidemia.2,5 A highcarbohydrate meal has been described to increase oxidative stress and favor proinflammatory effects. 5Several in vivo studies have found impaired nitric oxide (NO)-mediated endothelial function during acute episodes of hyperglycemia.6-10 NO is a key endothelium-derived relaxing factor and plays a pivotal role in the maintenance of basal vascular tone and vascular responses to dilative stimuli. [11][12][13] NO acts to negate the actions of endothelium-derived contracting factors such as angiotensin II and endothelin-1 (ET-1), as well as inhibit platelet aggregability 11-13 and endothelial activation.11-13 Therefore, reduced NO bioavailability may contribute to the onset and progression of endothelial dysfunction, including impaired vasodilative and increased adhesive properties, leading to atherogenesis.11-13 Additionally, endothelium-derived NO may act to regulate arterial stiffness and wave reflec-

No abstract

No abstract

No abstract