Institution
University of Milan
Education•Milan, Italy•
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.
Topics: Population, Medicine, Cancer, Blood pressure, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The role of the Tear Film and Ocular Surface Society (TFOS) Dry Eye Workshop (DEWS) II Diagnostic Methodology Subcommittee was to identify tests used to diagnose and monitor dry eye disease (DED) to identify those most appropriate to fulfil the definition of DED and its sub-classifications.
Abstract: The role of the Tear Film and Ocular Surface Society (TFOS) Dry Eye Workshop (DEWS) II Diagnostic Methodology Subcommittee was 1) to identify tests used to diagnose and monitor dry eye disease (DED), 2) to identify those most appropriate to fulfil the definition of DED and its sub-classifications, 3) to propose the most appropriate order and technique to conduct these tests in a clinical setting, and 4) to provide a differential diagnosis for DED and distinguish conditions where DED is a comorbidity. Prior to diagnosis, it is important to exclude conditions that can mimic DED with the aid of triaging questions. Symptom screening with the DEQ-5 or OSDI confirms that a patient might have DED and triggers the conduct of diagnostic tests of (ideally non-invasive) breakup time, osmolarity and ocular surface staining with fluorescein and lissamine green (observing the cornea, conjunctiva and eyelid margin). Meibomian gland dysfunction, lipid thickness/dynamics and tear volume assessment and their severity allow sub-classification of DED (as predominantly evaporative or aqueous deficient) which informs the management of DED. Videos of these diagnostic and sub-classification techniques are available on the TFOS website. It is envisaged that the identification of the key tests to diagnose and monitor DED and its sub-classifications will inform future epidemiological studies and management clinical trials, improving comparability, and enabling identification of the sub-classification of DED in which different management strategies are most efficacious.
1,152 citations
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University of Milan1, Instituto Português de Oncologia Francisco Gentil2, Curie Institute3, Leiden University Medical Center4, Vienna General Hospital5, University College London6, Leiden University7, Institut Jules Bordet8, Netherlands Cancer Institute9, Turku University Hospital10, University of Oxford11, University of Mannheim12, Ludwig Maximilian University of Munich13, Helsinki University Central Hospital14, The Royal Marsden NHS Foundation Trust15, Institute of Cancer Research16, University Medical Center Groningen17, Radboud University Nijmegen18, Institut Gustave Roussy19, Tel Aviv Sourasky Medical Center20, University Hospital of Lausanne21, University of Bologna22, University of Turin23, Weston Park Hospital24, Aarhus University Hospital25, Katholieke Universiteit Leuven26, Erasmus University Rotterdam27, Oslo University Hospital28, University College Hospital29, Claude Bernard University Lyon 130
1,150 citations
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TL;DR: Findings show that the BMP–BMPR signalling system—which controls the activity of normal brain stem cells—may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
Abstract: Transformed, oncogenic precursors, possessing both defining neural-stem-cell properties and the ability to initiate intracerebral tumours, have been identified in human brain cancers. Here we report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, trigger a significant reduction in the stem-like, tumour-initiating precursors of human glioblastomas (GBMs). Transient in vitro exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most importantly, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality that occur in 100% of mice after intracerebral grafting of human GBM cells. We demonstrate that BMPs activate their cognate receptors (BMPRs) and trigger the Smad signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation, and increased expression of markers of neural differentiation, with no effect on cell viability. The concomitant reduction in clonogenic ability, in the size of the CD133+ population and in the growth kinetics of GBM cells indicates that BMP4 reduces the tumour-initiating cell pool of GBMs. These findings show that the BMP-BMPR signalling system--which controls the activity of normal brain stem cells--may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and the results also identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
1,138 citations
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Queensland University of Technology1, Eindhoven University of Technology2, Capgemini3, University of Rome Tor Vergata4, Humboldt University of Berlin5, Software AG6, University of Padua7, Polytechnic University of Catalonia8, Hewlett-Packard9, Ghent University10, New Mexico State University11, IBM12, University of Milan13, University of Tartu14, University of Vienna15, Technical University of Lisbon16, Telecom SudParis17, Rabobank18, Infosys19, University of Calabria20, Fujitsu21, Pennsylvania State University22, University of Bari23, University of Bologna24, Vienna University of Economics and Business25, Free University of Bozen-Bolzano26, Stevens Institute of Technology27, Indian Council of Agricultural Research28, Pontifical Catholic University of Chile29, University of Haifa30, Ulsan National Institute of Science and Technology31, Cranfield University32, Katholieke Universiteit Leuven33, Deloitte34, Tsinghua University35, University of Innsbruck36, Hasso Plattner Institute37
TL;DR: This manifesto hopes to serve as a guide for software developers, scientists, consultants, business managers, and end-users to increase the maturity of process mining as a new tool to improve the design, control, and support of operational business processes.
Abstract: Process mining techniques are able to extract knowledge from event logs commonly available in today’s information systems. These techniques provide new means to discover, monitor, and improve processes in a variety of application domains. There are two main drivers for the growing interest in process mining. On the one hand, more and more events are being recorded, thus, providing detailed information about the history of processes. On the other hand, there is a need to improve and support business processes in competitive and rapidly changing environments. This manifesto is created by the IEEE Task Force on Process Mining and aims to promote the topic of process mining. Moreover, by defining a set of guiding principles and listing important challenges, this manifesto hopes to serve as a guide for software developers, scientists, consultants, business managers, and end-users. The goal is to increase the maturity of process mining as a new tool to improve the (re)design, control, and support of operational business processes.
1,135 citations
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TL;DR: It is shown that coactivation of the AMPA/kainate and metabotropic glutamate receptors (mGluRs) on astrocytes stimulates these cells to release glutamate through a Ca2+-dependent process mediated by prostaglandins, revealing a new pathway of regulated transmitter release from astroCytes and outlining the existence of an integrated glutamatergic cross-talk between neurons and astroicytes in situ.
Abstract: Astrocytes in the brain form an intimately associated network with neurons. They respond to neuronal activity and synaptically released glutamate by raising intracellular calcium concentration ([Ca2+]i)1,2 which could represent the start of back-signalling to neurons3,4,5. Here we show that coactivation of the AMPA/kainate and metabotropic glutamate receptors (mGluRs) on astrocytes stimulates these cells to release glutamate through a Ca2+-dependent process mediated by prostaglandins. Pharmacological inhibition of prostaglandin synthesis prevents glutamate release, whereas application of prostaglandins (in particular PGE2) mimics and occludes the releasing action of GluR agonists. PGE2 promotes Ca2+-dependent glutamate release from cultured astrocytes and also from acute brain slices under conditions that suppress neuronal exocytotic release. When applied to the CA1 hippocampal region, PGE2 induces increases in [Ca2+]i both in astrocytes and in neurons. The [Ca2+]i increase in neurons is mediated by glutamate released from astrocytes, because it is abolished by GluR antagonists. Our results reveal a new pathway of regulated transmitter release from astrocytes and outline the existence of an integrated glutamatergic cross-talk between neurons and astrocytes in situ that may play critical roles in synaptic plasticity and in neurotoxicity.
1,134 citations
Authors
Showing all 58902 results
Name | H-index | Papers | Citations |
---|---|---|---|
Yi Cui | 220 | 1015 | 199725 |
Peter J. Barnes | 194 | 1530 | 166618 |
Thomas C. Südhof | 191 | 653 | 118007 |
Charles A. Dinarello | 190 | 1058 | 139668 |
Alberto Mantovani | 183 | 1397 | 163826 |
John J.V. McMurray | 178 | 1389 | 184502 |
Giuseppe Remuzzi | 172 | 1226 | 160440 |
Russel J. Reiter | 169 | 1646 | 121010 |
Jean Louis Vincent | 161 | 1667 | 163721 |
Tobin J. Marks | 159 | 1621 | 111604 |
Tomas Hökfelt | 158 | 1033 | 95979 |
José Baselga | 156 | 707 | 122498 |
Naveed Sattar | 155 | 1326 | 116368 |
Silvia Franceschi | 155 | 1340 | 112504 |
Frederik Barkhof | 154 | 1449 | 104982 |