University of Milano-Bicocca

About: University of Milano-Bicocca is a education organization based out in Milan, Italy. It is known for research contribution in the topics: Population & Blood pressure. The organization has 8972 authors who have published 22322 publications receiving 620484 citations. The organization is also known as: Università degli Studi di Milano-Bicocca & Universita degli Studi di Milano-Bicocca.

Theoretical predictions for charm and bottom production at the LHC

Abstract: We present predictions for a variety of single-inclusive observables that stem from the production of charm and bottom quark pairs at the 7 TeV LHC. They are obtained within the FONLL semi-analytical framework, and with two "Monte Carlo + NLO" approaches, MC@NLO and POWHEG. Results are given for final states and acceptance cuts that are as close as possible to those used by experimental collaborations and, where feasible, are compared to LHC data.

A soluble form of the receptor for advanced glycation endproducts (RAGE) is produced by proteolytic cleavage of the membrane-bound form by the sheddase a disintegrin and metalloprotease 10 (ADAM10)

Abstract: The receptor for advanced glycation endproducts (RAGE) mediates responses to cell danger and stress. When bound by its many ligands (which include advanced glycation endproducts, certain members of the S100/calgranulin family, extracellular high-mobility group box 1, the integrin Mac-1, amyloid beta-peptide and fibrils), RAGE activates programs responsible for acute and chronic inflammation. RAGE is therefore also involved in cancer progression, diabetes, atherosclerosis, and Alzheimer's disease. RAGE has several isoforms deriving from alternative splicing, including a soluble form called endogenous secretory RAGE (esRAGE). We show here that most soluble RAGE, either produced by cell lines or present in human blood, is not recognized by an anti-esRAGE antibody. Cells transfected with the cDNA for full-length RAGE, and thus not expressing esRAGE, produce a form of soluble RAGE, cleaved RAGE (cRAGE) that derives from proteolytic cleavage of the membrane-bound molecules and acts as a decoy receptor. By screening chemical inhibitors and genetically modified mouse embryonic fibroblasts (MEFs), we identify the sheddase ADAM10 as a membrane protease responsible for RAGE cleavage. Binding of its ligand HMGB1 promotes RAGE shedding. Our data do not disprove the interpretation that high levels of soluble forms of RAGE protect against chronic inflammation, but rather suggest that they correlate with high levels of ongoing inflammation.

Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis.

Abstract: Prone position ventilation for acute hypoxemic respiratory failure (AHRF) improves oxygenation but not survival, except possibly when AHRF is severe. To determine effects of prone versus supine ventilation in AHRF and severe hypoxemia [partial pressure of arterial oxygen (PaO2)/inspired fraction of oxygen (FiO2) <100 mmHg] compared with moderate hypoxemia (100 mmHg ≤ PaO2/FiO2 ≤ 300 mmHg). Systematic review and meta-analysis. Electronic databases (to November 2009) and conference proceedings. Two authors independently selected and extracted data from parallel-group randomized controlled trials comparing prone with supine ventilation in mechanically ventilated adults or children with AHRF. Trialists provided subgroup data. The primary outcome was hospital mortality in patients with AHRF and PaO2/FiO2 <100 mmHg. Meta-analyses used study-level random-effects models. Ten trials (N = 1,867 patients) met inclusion criteria; most patients had acute lung injury. Methodological quality was relatively high. Prone ventilation reduced mortality in patients with PaO2/FiO2 <100 mmHg [risk ratio (RR) 0.84, 95% confidence interval (CI) 0.74–0.96; p = 0.01; seven trials, N = 555] but not in patients with PaO2/FiO2 ≥100 mmHg (RR 1.07, 95% CI 0.93–1.22; p = 0.36; seven trials, N = 1,169). Risk ratios differed significantly between subgroups (interaction p = 0.012). Post hoc analysis demonstrated statistically significant improved mortality in the more hypoxemic subgroup and significant differences between subgroups using a range of PaO2/FiO2 thresholds up to approximately 140 mmHg. Prone ventilation improved oxygenation by 27–39% over the first 3 days of therapy but increased the risks of pressure ulcers (RR 1.29, 95% CI 1.16–1.44), endotracheal tube obstruction (RR 1.58, 95% CI 1.24–2.01), and chest tube dislodgement (RR 3.14, 95% CI 1.02–9.69). There was no statistical between-trial heterogeneity for most clinical outcomes. Prone ventilation reduces mortality in patients with severe hypoxemia. Given associated risks, this approach should not be routine in all patients with AHRF, but may be considered for severely hypoxemic patients.

Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1

Abstract: Mitochondrial fusion depends on the dynamin-like guanosine triphosphatase OPA1, whose activity is controlled by proteolytic cleavage. Dysfunction of mitochondria induces OPA1 processing and results in mitochondrial fragmentation, allowing the selective removal of damaged mitochondria. In this study, we demonstrate that two classes of metallopeptidases regulate OPA1 cleavage in the mitochondrial inner membrane: isoenzymes of the adenosine triphosphate (ATP)-dependent matrix AAA (ATPase associated with diverse cellular activities [m-AAA]) protease, variable assemblies of the conserved subunits paraplegin, AFG3L1 and -2, and the ATP-independent peptidase OMA1. Functionally redundant isoenzymes of the m-AAA protease ensure the balanced accumulation of long and short isoforms of OPA1 required for mitochondrial fusion. The loss of AFG3L2 in mouse tissues, down-regulation of AFG3L1 and -2 in mouse embryonic fibroblasts, or the expression of a dominant-negative AFG3L2 variant in human cells decreases the stability of long OPA1 isoforms and induces OPA1 processing by OMA1. Moreover, cleavage by OMA1 causes the accumulation of short OPA1 variants if mitochondrial DNA is depleted or mitochondrial activities are impaired. Our findings link distinct peptidases to constitutive and induced OPA1 processing and shed new light on the pathogenesis of neurodegenerative disorders associated with mutations in m-AAA protease subunits.

Jet energy scale and resolution in the CMS experiment in pp collisions at 8 TeV

Abstract: Improved jet energy scale corrections, based on a data sample corresponding to an integrated luminosity of 19.7 fb^(-1) collected by the CMS experiment in proton-proton collisions at a center-of-mass energy of 8 TeV, are presented. The corrections as a function of pseudorapidity η and transverse momentum p_T are extracted from data and simulated events combining several channels and methods. They account successively for the effects of pileup, uniformity of the detector response, and residual data-simulation jet energy scale differences. Further corrections, depending on the jet flavor and distance parameter (jet size) R, are also presented. The jet energy resolution is measured in data and simulated events and is studied as a function of pileup, jet size, and jet flavor. Typical jet energy resolutions at the central rapidities are 15–20% at 30 GeV, about 10% at 100 GeV, and 5% at 1 TeV. The studies exploit events with dijet topology, as well as photon+jet, Z+jet and multijet events. Several new techniques are used to account for the various sources of jet energy scale corrections, and a full set of uncertainties, and their correlations, are provided. The final uncertainties on the jet energy scale are below 3% across the phase space considered by most analyses (p_T > 30 GeV and 0|η| 30 GeV is reached, when excluding the jet flavor uncertainties, which are provided separately for different jet flavors. A new benchmark for jet energy scale determination at hadron colliders is achieved with 0.32% uncertainty for jets with p_T of the order of 165–330 GeV, and |η| < 0.8.