University of Milan

About: University of Milan is a education organization based out in Milan, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 58413 authors who have published 139784 publications receiving 4636354 citations. The organization is also known as: Università degli Studi di Milano & Statale.

GW170817: Joint Constraint on the Neutron Star Equation of State from Multimessenger Observations

Abstract: Gravitational waves detected from the binary neutron star (NS) merger GW170817 constrained the NS equation of state by placing an upper bound on certain parameters describing the binary's tidal interactions. We show that the interpretation of the UV/optical/infrared counterpart of GW170817 with kilonova models, combined with new numerical relativity results, imply a complementary lower bound on the tidal deformability parameter. The joint constraints tentatively rule out both extremely stiff and soft NS equations of state.

An International Ki67 Reproducibility Study

Abstract: Uncontrolled proliferation is a key feature of malignancy. The nuclear proliferation marker Ki67 is of interest for various potential uses in the clinical management of breast cancer (eg, prognosis, prediction, and monitoring of response) (1–9). The most commonly used assay to assess Ki67 is immunohistochemical (IHC) staining with the MIB-1 antibody. However, interlaboratory methodology is inconsistent, and, despite the apparent prognostic utility of Ki67, routine use of this tumor biomarker has not been widely recommended by consensus guidelines panels such as that convened by the American Society of Clinical Oncology, mainly because of concerns regarding analytical validity (10). With the goal of harmonizing Ki67 analytical methodology, Dowsett et al., on behalf of the International Ki67 in Breast Cancer Working Group of the Breast International Group and North American Breast Cancer Group, provided an overview of the current state of the art of Ki67 evaluation and proposed a set of guidelines for analysis and reporting of Ki67 (1). Although those guidelines aimed to reduce preanalytical and analytical variations, the Working Group recognized that actual scoring procedures varied substantially, contributing to a lack of consensus regarding optimal cutoffs that should be applied in various research and clinical decision-making settings. This lack of consistency has prevented direct comparisons of Ki67 across laboratories and clinical trials. In an effort to harmonize Ki67 analysis, the Working Group studied intra- and interlaboratory reproducibility of IHC assays for Ki67 in breast cancer among a group of highly experienced pathology laboratories. A secondary aim was to identify key sources of variation, particularly those introduced by different scoring methodologies.

Searches for Lepton Flavor Violation in the Decays tau(+/-) -> e(+/-)gamma and tau(+/-) -> mu(+/-)gamma

Abstract: Searches for lepton-flavor-violating decays of a tau lepton to a lighter mass lepton and a photon have been performed with the entire data set of (963 +/- 7) x 10(6) tau decays collected by the BABAR detector near the Y(4S), Y(3S) and Y(2S) resonances. The searches yield no evidence of signals and we set upper limits on the branching fractions of B(tau(+/-) -> e(+/-)gamma) mu(+/-)gamma) < 4.4 X 10(-8) at 90% confidence level.

Acid sphingomyelinase activity triggers microparticle release from glial cells.

Abstract: We have earlier shown that microglia, the immune cells of the CNS, release microparticles from cell plasma membrane after ATP stimulation. These vesicles contain and release IL-1β, a crucial cytokine in CNS inflammatory events. In this study, we show that microparticles are also released by astrocytes and we get insights into the mechanism of their shedding. We show that, on activation of the ATP receptor P2X7, microparticle shedding is associated with rapid activation of acid sphingomyelinase, which moves to plasma membrane outer leaflet. ATP-induced shedding and IL-1β release are markedly reduced by the inhibition of acid sphingomyelinase, and completely blocked in glial cultures from acid sphingomyelinase knockout mice. We also show that p38 MAPK cascade is relevant for the whole process, as specific kinase inhibitors strongly reduce acid sphingomyelinase activation, microparticle shedding and IL-1β release. Our results represent the first demonstration that activation of acid sphingomyelinase is necessary and sufficient for microparticle release from glial cells and define key molecular effectors of microparticle formation and IL-1β release, thus, opening new strategies for the treatment of neuroinflammatory diseases.