88 research outputs found

    PCBs and PAHs in sea-surface microlayer and sub-surfacewater samples of the Venice Lagoon (Italy)

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    Polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs) are two classes of micropollutants intensively monitored and regulated due to their toxicity, persistency and wide diffusion. Their concentrations have been investigated in sea-microlayer (SML) and sub-surface water (SSW) samples collected at two sites of the Venice Lagoon, a fragile ecosystem highly influenced by industrial and anthropogenic emissions. The total PPCB concentration varies from 0.45 ng/l to 2.1 ng/l in SSW while a clear enrichment is observed in the SML, where it ranges from 1.2 ng/l to 10.5 ng/l. The total PPAH concentration shows marked differences between the two stations and varies from 12.4 ng/l to 266.8 ng/l in SSW; in SML it is more uniform and ranges from 19.6 ng/l to 178.9 ng/l. The enrichment factors are not larger than 1 for both pollutants in the dissolved phase, while they are most significant for the particulate phase (PPCB: 5–9; PPAH: 4–14). 2005 Elsevier Ltd. All rights reserved

    N-acetylcysteine reduces oxidative stress in sickle cell patients

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    Oxidative stress is of importance in the pathophysiology of sickle cell disease (SCD). In this open label randomized pilot study the effects of oral N-acetylcysteine (NAC) on phosphatidylserine (PS) expression as marker of cellular oxidative damage (primary end point), and markers of hemolysis, coagulation and endothelial activation and NAC tolerability (secondary end points) were studied. Eleven consecutive patients (ten homozygous [HbSS] sickle cell patients, one HbSβ0-thalassemia patient) were randomly assigned to treatment with either 1,200 or 2,400 mg NAC daily during 6 weeks. The data indicate an increment in whole blood glutathione levels and a decrease in erythrocyte outer membrane phosphatidylserine exposure, plasma levels of advanced glycation end-products (AGEs) and cell-free hemoglobin after 6 weeks of NAC treatment in both dose groups. One patient did not tolerate the 2,400 mg dose and continued with the 1,200 mg dose. During the study period, none of the patients experienced painful crises or other significant SCD or NAC related complications. These data indicate that N-acetylcysteine treatment of sickle cell patients may reduce SCD related oxidative stress

    Sequestration and Tissue Accumulation of Human Malaria Parasites: Can We Learn Anything from Rodent Models of Malaria?

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    The sequestration of Plasmodium falciparum–infected red blood cells (irbcs) in the microvasculature of organs is associated with severe disease; correspondingly, the molecular basis of irbc adherence is an active area of study. In contrast to P. falciparum, much less is known about sequestration in other Plasmodium parasites, including those species that are used as models to study severe malaria. Here, we review the cytoadherence properties of irbcs of the rodent parasite Plasmodium berghei ANKA, where schizonts demonstrate a clear sequestration phenotype. Real-time in vivo imaging of transgenic P. berghei parasites in rodents has revealed a CD36-dependent sequestration in lungs and adipose tissue. In the absence of direct orthologs of the P. falciparum proteins that mediate binding to human CD36, the P. berghei proteins and/or mechanisms of rodent CD36 binding are as yet unknown. In addition to CD36-dependent schizont sequestration, irbcs accumulate during severe disease in different tissues, including the brain. The role of sequestration is discussed in the context of disease as are the general (dis)similarities of P. berghei and P. falciparum sequestration

    n-Alkanes, PAHs and surfactants in the sea surface microlayer and sea water samples of the Gerlache Inlet sea (Antarctica)

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    Sea surface microlayer (SML) and sea water samples (SSW) collected in the Gerlache Inlet Sea (Antarctica) were analysed for n-alkanes and polycyclic aromatic hydrocarbons (PAHs). The SML is a potential enrichment site of hydrophobic organic compounds compared to the underlying water column. Total concentration ranges of n-alkanes and PAHs (dissolved and particulate) in subsurface water (−0.5 m depth) were 272– 553 ng l−1 (mean: 448 ng l−1) and 5.27–9.43 ng l−1 (mean: 7.06 ng l−1), respectively. In the SML, the concentration ranges of n-alkanes and PAHs were 353–968 ng l−1 (mean: 611 ng l−1) and 7.32–23.94 ng l−1 (mean: 13.22 ng l−1), respectively. To evaluate possible PAH contamination sources, specific PAH ratios were calculated. The ratios reflected a predominant petrogenic input. A characterisation of surface active substances was also performed on SML and SSW samples, both by gas bubble extraction, and by dynamic surface tension measurements. Results showed a good correlation between n-alkanes, PAHs and refractory organic matter

    Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients

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    Red blood cells (RBCs) enzymatically produce nitric oxide (NO) by a functional RBC-nitric oxide synthase (RBC-NOS). NO is a vascular key regulatory molecule. In RBCs its generation is complex and influenced by several factors, including insulin, acetylcholine, and calcium. NO availability is reduced in end-stage renal disease (ESRD) and associated with endothelial dysfunction. We previously demonstrated that, through increased phosphatidylserine membrane exposure, ESRD-RBCs augmented their adhesion to human cultured endothelium, in which NO bioavailability decreased. Since RBC-NOS-dependent NO production in ESRD is unknown, this study aimed to investigate RBC-NOS levels/activation, NO production/bioavailability in RBCs from healthy control subjects (C, N = 18) and ESRD patients (N = 27). Although RBC-NOS expression was lower in ESRD-RBCs, NO, cyclic guanosine monophosphate (cGMP), RBC-NOS Serine1177 phosphorylation level and eNOS/Calmodulin (CaM)/Heat Shock Protein-90 (HSP90) interaction levels were higher in ESRD-RBCs, indicating increased enzyme activation. Conversely, following RBCs stimulation with insulin or ionomycin, NO and cGMP levels were significantly lower in ESRD- than in C-RBCs, suggesting that uremia might reduce the RBC-NOS response to further stimuli. Additionally, the activity of multidrug-resistance-associated protein-4 (MRP4; cGMP-membrane transporter) was significantly lower in ESRD-RBCs, suggesting a possible compromised efflux of cGMP across the ESRD-RBCs membrane. This study for the first time showed highest basal RBC-NOS activation in ESRD-RBCs, possibly to reduce the negative impact of decreased NOS expression. It is further conceivable that high NO production only partially affects cell function of ESRD-RBCs maybe because in vivo they are unable to respond to physiologic stimuli, such as calcium and/or insulin

    Atmospheric PCB concentrations at Terra Nova Bay, Antarctica

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    Concentrations of gas-phase polychlorobiphenyls (PCBs) were studied over an austral summer at a site in Terra Nova Bay, Antarctica. Gas-phase concentrations of individual PCB congeners in the atmosphere of Terra Nova Bay ranged from below the detection limit to 0.25 pg m-3, with a mean concentration of åPCB of 1.06 pg m-3. The PCB profile was dominated by lower-chlorinated PCB congeners; in fact >78% of the total PCB content was due to congeners with 1-4 chlorine atoms and only about 10% with 5-7 chlorines, whereas higher-chlorinated PCB congeners were below detection limits. The mean åPCB concentration obtained in this study were lower than those reported in previous Antarctic studies. Temporal concentration profiles of åPCB do not correspond to seasonal temperature changes. In consideration of the low PCB concentrations observed, the studies with the wind roses, the regression between ln P(PCB) and T-1, and the distribution of congeners, we can hypothesize that PCB local source contributions are not very important, whereas long-distance transport is the prevalent factor bringing PCBs to Terra Nova Bay

    The policy of the United States towards Cuba from 1989-1996

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    In the immediate post-Cold War period, as the security rationale for the U.S. embargo disappeared, the United States tightened rather than eased sanctions on Cuba. This dissertation focuses on the competition between Congress and the executive for control of policy towards Cuba, and the domestic interests which shaped policymaking and led to the passage of two major pieces of legislation fiercely resisted by U.S. allies. The dissertation begins with an analysis of U.S. policy towards Cuba in the summer of 1989, before the collapse of communism in Eastern Europe. Five days of congressional hearings called by Representative George Crockett (D.Michigan) in his attempt to spark a reassessment of relations between the two countries form the basis for a review of policy over the preceding thirty years. The first chapter will also introduce the Cuban American National Foundation, the pre-eminent domestic interest group in U.S. policy towards Cuba in 1989-1996, and the U.S. campaign to have Cuba condemned for human rights violations at the United Nations Human Right Commission. The second chapter examines the policy debate in 1989-1992, focusing on the provision of information to Cubans, the intensification of economic sanctions, and the continuation of the human rights campaign. The third chapter analyses the role of migration from Cuba to the United States between 1959-1992, arguing the main objective of U.S. policy. Chapter four looks at continuity and change under the Clinton administration, and in particular at the administration’s handling of the rafter (migration) crisis of 1994 and the resulting agreements reached with the Cuban government. The primary focus of the fifth chapter will be the struggle between the executive and Congress over the Helms-Burton legislation, signed by Clinton in March 1996.EThOS - Electronic Theses Online ServiceGBUnited Kingdo
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