Around the world, there is a growing increase in biofuels consumption, mainly ethanol and biodiesel as well as their blends with diesel that reduce the cost impact of biofuels while retaining some of the advantages of the biofuels. This increase is due to several factors like decreasing the dependence on imported petroleum; providing a market for the excess production of vegetable oils and animal fats; using renewable and biodegradable fuels; reducing global warming due to its closed carbon cycle by CO2 recycling; increasing lubricity; and reducing substantially the exhaust emissions of carbon monoxide, unburned hydrocarbons, and particulate emissions from diesel engines. However, there are major drawbacks in the use of biofuel blends as NOx tends to be higher, the intervals of motor parts replacement such as fuel filters are reduced and degradation by chronic exposure of varnish deposits in fuel tanks and fuel lines, paint, concrete, and paving occurs as some materials are incompatible. Here, fuel additives become indispensable tools not only to decrease these drawbacks but also to produce specified products that meet international and regional standards like EN 14214, ASTM D 6751, and DIN EN 14214, allowing the fuels trade to take place. Additives improve ignition and combustion efficiency, stabilize fuel mixtures, protect the motor from abrasion and wax deposition, and reduce pollutant emissions, among other features. Two basic trends are becoming more relevant:  the progressive reduction of sulfur content and the increased use of biofuels. Several additives' compositions may be used as long as they keep the basic chemical functions that are active.

The results suggest that the nature of children's loneliness may be affected by the broad socio-cultural context.

1 We aimed to functionally characterize endothelin (ET) receptors in the rat carotid artery. mRNA and protein expressions of both ET A and ET B receptors, evaluated by reverse transcriptionpolymerase chain reaction (RT-PCR) and Western immunoblotting, were detected in carotid segments. Immunohistochemical assays showed that ET B receptors are expressed in the endothelium and smooth muscle cells, while ET A receptors are expressed only in the smooth muscle cells. In endothelium-denuded vessels, levels of ET B receptor mRNA were reduced. 2 Vascular reactivity experiments, using standard muscle bath procedures, showed that ET-1 induces contraction in endothelium-intact and -denuded carotid rings in a concentration-dependent manner. Endothelial removal enhanced ET-1-induced contraction. BQ123 and BQ788, selective antagonists for ET A and ET B receptors, respectively, produced concentration-dependent rightward displacements of the ET-1 concentration-response curves. 3 IRL1620, a selective agonist for ET B receptors, induced a slight vasoconstriction that was abolished by BQ788, but not affected by BQ123. IRL1620-induced contraction was augmented after endothelium removal. 4 ET-1 concentration dependently relaxed phenylephrine-precontracted rings with intact endothelium. The relaxation was augmented in the presence of BQ123, reduced in the presence of BQ788 and completely abolished after endothelium removal. IRL1620 induced vasorelaxation that was abolished by BQ788 and endothelium removal, but not affected by BQ123. 5 Preincubation of intact rings with N G -nitro-L-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), indomethacin or tetraethylammonium (TEA) reduced IRL1620-induced relaxation. The combination of L-NAME, indomethacin and TEA completely abolished IRL1620-induced relaxation while sulfaphenazole did not affect this response. 4-aminopyridine (4-AP), but not apamin, glibenclamide or charybdotoxin, reduced IRL1620-induced relaxation. 6 The major finding of this work is that it firstly demonstrated functionally the existence of both ET A and ET B vasoconstrictor receptors located on the smooth muscle of rat carotid arteries and endothelial ET B receptors that mediated vasorelaxation via NO-cGMP pathway, vasodilator cyclooxygenase product(s) and the activation of voltage-dependent K þ channels.

Adipocytes produce adipokines, including chemerin, a chemoattractant that mediates effects through its ChemR23 receptor. Chemerin has been linked to endothelial dysfunction and vascular injury in pathological conditions, such as obesity, diabetes mellitus, and hypertension. Molecular mechanisms underlying this are elusive. Here we assessed whether chemerin through redox-sensitive signaling influences molecular processes associated with vascular growth, apoptosis, and inflammation. Human microvascular endothelial cells and vascular smooth muscle cells were stimulated with chemerin (50 ng/mL). Chemerin increased generation of reactive oxygen species and phosphorylation of mitogen-activated protein kinases, effects that were inhibited by ML171, GKT137831 (Nox inhibitors), and N-acetylcysteine (reactive oxygen species scavenger). Chemerin increased mRNA expression of proinflammatory mediators in vascular cells and increased monocyte-to-endothelial cell attachment. In human vascular smooth muscle cells, chemerin induced phosphorylation of mitogen-activated protein kinases and stimulated proliferation (increased proliferating cell nuclear antigen expression [proliferation marker] and BrdU incorporation [proliferation assay]). Chemerin decreased phosphatidylinositol 3-kinase/protein kinase B activation and increased TUNEL-positive human vascular smooth muscle cells. In human microvascular endothelial cells, chemerin reduced endothelial nitric oxide synthase activity and nitric oxide production. Adipocyte-conditioned medium from obese/diabetic mice (db/db), which have elevated chemerin levels, increased reactive oxygen species generation in vascular smooth muscle cells, whereas adipocyte-conditioned medium from control mice had no effect. Chemerin actions were blocked by CCX 832, a ChemR23 inhibitor. Our data demonstrate that chemerin, through Nox activation and redox-sensitive mitogen-activated protein kinases signaling, exerts proapoptotic, proinflammatory, and proliferative effects in human vascular cells. These findings elucidate some molecular mechanisms through chemerin, which is increased in obesity, whereby adipocytes may influence vascular function. We identify chemerin as a novel vasoactive adipokine, which may be important in obesity-related vascular injury.

The purpose of the present study was to examine relations between self-perceptions of competence and social, behavioural, and school adjustment in Brazilian, Canadian, Chinese, and Italian children. Self-perception data were collected through children’s self-reports. Information about social behaviours, peer acceptance, and school achievement was obtained from peer assessments and teacher ratings. Multi-group analyses revealed similar patterns of relations between self-perceptions in scholastic and general self-worth domains and social and school performance in the four samples. However, the relations between self-perceptions of social competence and shyness and academic achievement were different across these samples. Self-perceptions of social competence was negatively associated with shyness in Brazilian, Canadian, and Italian children, but not in the Chinese children, and positively associated with academic achievement in Canadian and Chinese children, but not in Brazilian and Italian children. Similarities and differences in the patterns of relations between self-perceptions and social and school adjustment across cultures indicate that the self system may be a culture-general as well as culture-specific phenomenon.

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