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- Aamodt, K., et al.
(författare)
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The ALICE experiment at the CERN LHC
- 2008
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Ingår i: Journal of Instrumentation. - 1748-0221. ; 3:S08002
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Forskningsöversikt (refereegranskat)abstract
- ALICE (A Large Ion Collider Experiment) is a general-purpose, heavy-ion detector at the CERN LHC which focuses on QCD, the strong-interaction sector of the Standard Model. It is designed to address the physics of strongly interacting matter and the quark-gluon plasma at extreme values of energy density and temperature in nucleus-nucleus collisions. Besides running with Pb ions, the physics programme includes collisions with lighter ions, lower energy running and dedicated proton-nucleus runs. ALICE will also take data with proton beams at the top LHC energy to collect reference data for the heavy-ion programme and to address several QCD topics for which ALICE is complementary to the other LHC detectors. The ALICE detector has been built by a collaboration including currently over 1000 physicists and engineers from 105 Institutes in 30 countries, Its overall dimensions are 16 x 16 x 26 m(3) with a total weight of approximately 10 000 t. The experiment consists of 18 different detector systems each with its own specific technology choice and design constraints, driven both by the physics requirements and the experimental conditions expected at LHC. The most stringent design constraint is to cope with the extreme particle multiplicity anticipated in central Pb-Pb collisions. The different subsystems were optimized to provide high-momentum resolution as well as excellent Particle Identification (PID) over a broad range in momentum, up to the highest multiplicities predicted for LHC. This will allow for comprehensive studies of hadrons, electrons, muons, and photons produced in the collision of heavy nuclei. Most detector systems are scheduled to be installed and ready for data taking by mid-2008 when the LHC is scheduled to start operation, with the exception of parts of the Photon Spectrometer (PHOS), Transition Radiation Detector (TRD) and Electro Magnetic Calorimeter (EMCal). These detectors will be completed for the high-luminosity ion run expected in 2010. This paper describes in detail the detector components as installed for the first data taking in the summer of 2008.
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| 2. |
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| 3. |
- Vanzetto, S, et al.
(författare)
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Epigenetic modulation in obsessive-compulsive disorder: Methylation and hydroxymethylation of the bdnf gene exon I promoter
- 2021
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Ingår i: EUROPEAN PSYCHIATRY. - : Royal College of Psychiatrists. - 0924-9338 .- 1778-3585. ; 64, s. S124-S124
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Several evidence recognizes Brain Derived Neurotrophic Factor (BDNF) as a promising biomarker in the pathophysiology of psychiatric disorders, including Obsessive-Compulsive Disorder (OCD), considering the involvement of epigenetic regulation in BDNF altered expression.ObjectivesThis study aims to investigate, in a sample of OCD patients, the epigenetic modulation in terms of levels of methylation and hydroxymethylation on the BDNF gene exon I promoter.MethodsFifty OCD patients, recruited from Psychiatry Unit 2, Sacco University Hospital in Milan and fifty healthy controls, comparable by age and gender. Saliva samples were collected by oral swab and epigenetic analysis were performed at the University of Teramo. Statistical analyses were performed with t test with Bonferroni correction.ResultsData analysis showed a significant decrease in 5-methyl cytosine levels (5mC) (mean OCD: 1.221%; mean CTRL: 1.784%; p < 0.001) and a significant increase in 5-Hydroxy-methyl cytosine levels (5hmC) (mean OCD: 1.018%; mean CTRL: 0.527% p< 0.0001) in BDNF gene exon I promoter of OCD patients compared to controls. Regarding 5mC of site 3 and 5hmC of site 1 and 2 of the exon I promoter CpG islands, no statistical significance was found.ConclusionsPresent results showed significant differences in epigenetic modulation of BDNF gene, which might not be univocally interpreted. They could represent an intrinsic OCD characteristic or the effect of antidepressant drugs, assumed by all recruited patients. Further studies, comparing OCD subjects in treatment vs drug-free, are necessary to define BDNF epigenetic modulation role and its possible use as biomarker in the characterization of OCD.DisclosureNo significant relationships.
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| 5. |
- Vismara, M, et al.
(författare)
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Peripheral Biomarkers in DSM-5 Anxiety Disorders: An Updated Overview
- 2020
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Ingår i: Brain sciences. - : MDPI AG. - 2076-3425. ; 10:8
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Tidskriftsartikel (refereegranskat)abstract
- Anxiety disorders are prevalent and highly disabling mental disorders. In recent years, intensive efforts focused on the search for potential neuroimaging, genetic, and peripheral biomarkers in order to better understand the pathophysiology of these disorders, support their diagnosis, and characterize the treatment response. Of note, peripheral blood biomarkers, as surrogates for the central nervous system, represent a promising instrument to characterize psychiatric disorders, although their role has not been extensively applied to clinical practice. In this report, the state of the art on peripheral biomarkers of DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th edition) Anxiety Disorders is presented, in order to examine their role in the pathogenesis of these conditions and their potential application for diagnosis and treatment. Available data on the cerebrospinal fluid and blood-based biomarkers related to neurotransmitters, neuropeptides, the hypothalamic–pituitary–adrenal axis, neurotrophic factors, and the inflammation and immune system are reviewed. Despite the wide scientific literature and the promising results in the field, only a few of the proposed peripheral biomarkers have been defined as a specific diagnostic instrument or have been identified as a guide in the treatment response to DSM-5 Anxiety Disorders. Therefore, further investigations are needed to provide new biological insights into the pathogenesis of anxiety disorders, to help in their diagnosis, and to tailor a treatment.
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