403 research outputs found
Omega-3 Fatty Acids and PPARγ in Cancer
Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator receptor activator (PPAR)γ and, due to the effects of PPARγ on cell proliferation, survival, and differentiation, are potential anticancer agents. Dietary intake of omega-3 PUFAs has been associated with a reduced risk of certain cancers in human populations and in animal models. In vitro studies have shown that omega-3 PUFAs inhibit cell proliferation and induce apoptosis in cancer cells through various pathways but one of which involves PPARγ activation. The differential activation of PPARγ and PPARγ-regulated genes by specific dietary fatty acids may be central to their distinct roles in cancer. This review summarizes studies relating PUFAs to PPARγ and cancer and offers a new paradigm relating an n-3 PUFA through PPARγ to the expression of the cell surface proteoglycan, syndecan-1, and to the death of cancer cells
National Soils Database
End of project reportThe objectives of the National Soils Database project were fourfold. The first was to generate a national database of soil geochemistry to complete the work that commenced with a survey of the South East of Ireland carried out in 1995 and 1996 by Teagasc (McGrath and McCormack, 1999). Secondly, to produce point and interpolated spatial distribution maps of major, minor and trace elements and to interpret these with respect to underlying parent material, glacial geology, land use and possible anthropogenic effects. A third objective was to investigate the microbial community structure in a range of soil types to determine the relationship between soil microbiology and chemistry. The final objective was to establish a National Soils Archive
Multinet : enabler for next generation enterprise wireless services
Wireless communications are currently experiencing a fast migration toward the beyond third-generation (B3G)/fourth generation (4G) era. This represents a generational change in wireless systems: new capabilities related to mobility and new services support is required and new concepts as individual-centric, user-centric or ambient-aware communications are included. One of the main restrictions associated to wireless technology is mobility management, this feature was not considered in the design phase; for this reason, a complete solution is not already found, although different solutions are proposed and are being proposed. In MULTINET project, features as mobility and multihoming are applied to wireless network to provide the necessary network and application functionality enhancements for seamless data communication mobility considering end-user scenario and preferences. The aim of this paper is to show the benefits of these functionalities from the Service Providers and final User point of view
Structural identification of oxidized acyl-phosphatidylcholines that induce platelet activation
Oxidation of low-density lipoprotein (LDL) generates proinflammatory and prothrombotic mediators that may play a crucial role in cardiovascular and inflammatory diseases. In order to study platelet-activating components of oxidized LDL 1-stearoyl-2-arachidonoyl-sn-glycero-3- phosphocholine, a representative of the major phospholipid species in LDL, the 1-acyl-phosphatidylcholines (PC), was oxidized by CuCl2 and H2O2. After separation by high-performance liquid chromatography, three compounds were detected which induced platelet shape change at low micromolar concentrations. Platelet activation by these compounds was distinct from the pathways stimulated by platelet-activating factor, lysophosphatidic acid, lyso-PC and thromboxane A(2), as evidenced by the use of specific receptor antagonists. Further analyses of the oxidized phospholipids by electrospray ionization mass spectrometry structurally identified them as 1-stearoyl-2-azelaoyl-sn-glycero-3-phosphocholine (m/z 694; SAzPC), 1-stearoyl-2-glutaroyl-snglycero-3- phosphocholine (m/z 638; SGPC), and 1-stearoyl-2-( 5-oxovaleroyl)-sn-glycero-3-phosphocholine (m/z 622; SOVPC). These observations demonstrate that novel 1-acyl-PC which had previously been found to stimulate interaction of monocytes with endothelial cells also induce platelet activation, a central step in acute thrombogenic and atherogenic processes. Copyright (C) 2005 S. Karger AG, Basel
Regulation of platelet-activating-factor receptors and the desensitization response in polymorphonuclear neutrophils
Population assessment of future trajectories in coronary heart disease mortality.
Background:
Coronary heart disease (CHD) mortality rates have been decreasing in Iceland since the 1980s, largely
reflecting improvements in cardiovascular risk factors. The purpose of this study was to predict future CHD mortality in
Iceland based on potential risk factor trends.
Methods and findings:
The previously validated IMPACT model was used to predict changes in CHD mortality between 2010 and 2040 among the projected population of Iceland aged 25–74. Calculations were based on combining: i) data on population numbers and projections (Statistics Iceland), ii) population risk factor levels and projections (Refine Reykjavik study), and iii) effectiveness of specific risk factor reductions (published meta-analyses). Projections for three contrasting
scenarios were compared: 1) If the historical risk factor trends of past 30 years were to continue, the declining death rates of past decades would level off, reflecting population ageing. 2) If recent trends in risk factors (past 5 years) continue, this would result in a death rate increasing from 49 to 70 per 100,000. This would reflect a recent plateau in previously falling cholesterol levels and recent rapid increases in obesity and diabetes prevalence. 3) Assuming that in 2040 the entire population enjoys optimal risk factor levels observed in low risk cohorts, this would prevent almost all premature CHD deaths before 2040.
Conclusions:
The potential increase in CHD deaths with recent trends in risk factor levels is alarming both for Iceland and
probably for comparable Western populations. However, our results show considerable room for reducing CHD mortality.
Achieving the best case scenario could eradicate premature CHD deaths by 2040. Public health policy interventions based
on these predictions may provide a cost effective means of reducing CHD mortality in the future
Binding and metabolism of platelet-activating factor by human neutrophils.
Human polymorphonuclear neutrophils rapidly incorporated radiolabeled platelet-activating factor, 1-O-[hexadecyl-9, 10-3H2]-2-acetyl-sn-glycero-3-phosphocholine ([3H]PAF), and then metabolized it into its sn-2-fatty acyl derivative. Fractionation of radiolabel-pretreated cells over Percoll gradients revealed that virtually all of the intact [3H]PAF was located in nongranule membranes that were enriched with alkaline phosphatase and cell surface glycoproteins. While still membrane associated, the ligand was rapidly converted to its acyl derivative and then more slowly transferred to specific granules and, to a lesser extent, azurophilic granules. In contrast, neutrophils did not metabolize [3H]PAF at 4 degrees C but rather gradually accumulated it in their alkaline phosphatase-enriched membrane subfractions. These same subfractions contained receptors for the ligand, as determined by their capacity to bind [3H]PAF specifically. Binding was readily saturated, partially reversible, and fit a two receptor model; dissociation constant (Kd) values for high and low affinity sites were 0.2 and 500 nM, respectively. Receptors with similar affinities were detected in whole cells. Furthermore, the potencies of several structural analogues in inhibiting binding of [3H]PAF to membranes correlated closely with their respective potencies in stimulating degranulation responses. Finally, quantitative studies suggested all or most of the cell's receptors were membrane associated. We conclude that PAF rapidly enters cellular membranes to bind with specific receptors that trigger function. The intramembranous ligand is also deacetylated, acylated, and then transferred to granules. This metabolism may be sufficiently rapid to limit ligand-receptor binding and distort quantitative analyses of receptors
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