Rio de Janeiro State University

About: Rio de Janeiro State University is a education organization based out in Rio de Janeiro, Brazil. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 16631 authors who have published 30919 publications receiving 465753 citations. The organization is also known as: UERJ & Rio de Janeiro State University.

Search for narrow resonances in dilepton mass spectra in pp collisions at s=7TeV

Abstract: A search for narrow, high-mass resonances decaying to electron or muon pairs has been performed using pp collision data collected at sqrt(s)=7 TeV by the CMS experiment in 2011. The data sample corresponds to an integrated luminosity of approximately 5 inverse femtobarns. The event yields observed in the signal regions are consistent with predictions of the standard model backgrounds, and upper limits on the cross section times branching fraction for a resonance decaying to dileptons are extracted from a shape analysis of the dilepton invariant mass distribution. The resulting mass limits at 95% confidence level are 2330 GeV for the Z' in the Sequential Standard Model, 2000 GeV for the superstring-inspired Z'(psi) resonance, 890 (540) GeV for the Stueckelberg extension Z'(St) with the mass parameter epsilon=0.06 (0.04), and 2140 (1810) GeV for Kaluza--Klein gravitons with the coupling parameter k/Mbar(Pl) of 0.10 (0.05). These limits are the most stringent to date.

Aspirin-triggered lipoxin A4 blocks reactive oxygen species generation in endothelial cells: A novel antioxidative mechanism

Abstract: Lipoxins and their aspirin-triggered carbon-15 epimers have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on cardiovascular diseases such as hypertension, atherosclerosis, and heart failure has not been investigated. One of the major features shared by these pathological conditions is the increased production of reactive oxygen species (ROS) generated by vascular NAD(P)H oxidase activation. In this study, we have examined whether an aspirin-triggered lipoxin A (4) analog (ATL-1) modulates ROS generation in endothelial cells (EC). Pre-treatment of EC with ATL-1 (1 - 100 nM) completely blocked ROS production triggered by different agents, as assessed by dihydrorhodamine 123 and hydroethidine. Furthermore, ATL-1 inhibited the phosphorylation and translocation of the cytosplamic NAD(P)H oxidase subunit p47 (phox) to the cell membrane as well as NAD(P)H oxidase activity. Western blot and immunofluorescence microscopy analyses showed that ATL-1 (100 nM) impaired the redox-sensitive activation of the transcriptional factor NF- kappaB, a critical step in several events associated to vascular pathologies. These results demonstrate that ATL-1 suppresses NAD(P)H oxidase-mediated ROS generation in EC, strongly indicating that lipoxins may play a protective role against the development and progression of cardiovascular diseases.

Food as medicine: targeting the uraemic phenotype in chronic kidney disease.

Abstract: The observation that unhealthy diets (those that are low in whole grains, fruits and vegetables, and high in sugar, salt, saturated fat and ultra-processed foods) are a major risk factor for poor health outcomes has boosted interest in the concept of 'food as medicine'. This concept is especially relevant to metabolic diseases, such as chronic kidney disease (CKD), in which dietary approaches are already used to ameliorate metabolic and nutritional complications. Increased awareness that toxic uraemic metabolites originate not only from intermediary metabolism but also from gut microbial metabolism, which is directly influenced by diet, has fuelled interest in the potential of 'food as medicine' approaches in CKD beyond the current strategies of protein, sodium and phosphate restriction. Bioactive nutrients can alter the composition and metabolism of the microbiota, act as modulators of transcription factors involved in inflammation and oxidative stress, mitigate mitochondrial dysfunction, act as senolytics and impact the epigenome by altering one-carbon metabolism. As gut dysbiosis, inflammation, oxidative stress, mitochondrial dysfunction, premature ageing and epigenetic changes are common features of CKD, these findings suggest that tailored, healthy diets that include bioactive nutrients as part of the foodome could potentially be used to prevent and treat CKD and its complications.