148 research outputs found
l W nu production at CLIC: a window to TeV scale non-decoupled neutrinos
We discuss single heavy neutrino production e+ e- -> N nu -> l W nu, l = e,
mu, tau, at a future high energy collider like CLIC, with a centre of mass
energy of 3 TeV. This process could allow to detect heavy neutrinos with masses
of 1-2 TeV if their coupling to the electron V_eN is in the range 0.004-0.01.
We study the dependence of the limits on the heavy neutrino mass and emphasise
the crucial role of lepton flavour in the discovery of a positive signal at
CLIC energy. We present strategies to determine heavy neutrino properties once
they are discovered, namely their Dirac or Majorana character and the size and
chirality of their charged current couplings. Conversely, if no signal is
found, the bound V_eN < 0.002-0.006 would be set for masses of 1-2 TeV,
improving the present limit up to a factor of 30. We also extend previous work
examining in detail the flavour and mass dependence of the corresponding limits
at ILC, as well as the determination of heavy neutrino properties if they are
discovered at this collider.Comment: LaTeX 32 pages. Added comments and references. Matches version to
appear in JHE
Occurrence of immature forms of culicids (Insecta: Diptera) in the northeastern region of Brazil
Understanding and examining teacher resilience from multiple perspectives
In this chapter, I argue that differing conceptualisations of the construct of resilience shape and enrich the research questions and methodology used to examine it. In addition, the conceptual focus has implications for questions such as whose responsibility it is for the development of resilience. Research conducted within two Australian projects, Keeping Cool and BRiTE (Building Resilience in Teacher Education) is used as an illustration of the impact of a changing conceptual focus. For example, beginning with a psychological perspective led to an examination of risk and protective factors for individuals. More contextual approaches involved a comparison of countries. Recent systemic views support a model that encompasses both personal and contextual characteristics, as well as strategies used and outcomes achieved. It is argued that taking multiple perspectives in this programme of work has enabled the incorporation of a broad range of research methods and findings, and contributed to a deeper understanding of the construct of teacher resilience
Pairing of Homologous Regions in the Mouse Genome Is Associated with Transcription but Not Imprinting Status
This work was funded by the BBSRC, grant BB/H088071/1 (www.bbsrc.ac.uk), MRC, grant G0700760 (www.mrc.ac.uk), Wellcome Trust, grant 095645/Z/11/Z (www.wellcome.ac.uk) and the EU through EpiGeneSys (www.epigenesys.eu) and Blueprint (www.blueprint-epigenome.eu). C.K. was funded by the DFG, personal fellowship KR 3317/2-1 (www.dfg.de) and CTR, personal short term fellowship (www.trophoblast.cam.ac.uk). M.J.H. received funding through grant NCI/NIH 2RO1 CA089426 (www.nih.gov)
Chronic widespread musculoskeletal pain, fatigue, depression and disordered sleep in chronic post-SARS syndrome; a case-controlled study
<p>Abstract</p> <p>Background</p> <p>The long term adverse effects of Severe Acute Respiratory Syndrome (SARS), a viral disease, are poorly understood.</p> <p>Methods</p> <p>Sleep physiology, somatic and mood symptoms of 22 Toronto subjects, 21 of whom were healthcare workers, (19 females, 3 males, mean age 46.29 yrs.+/- 11.02) who remained unable to return to their former occupation (mean 19.8 months, range: 13 to 36 months following SARS) were compared to 7 healthy female subjects. Because of their clinical similarities to patients with fibromyalgia syndrome (FMS) these post-SARS subjects were similarly compared to 21 drug free female patients, (mean age 42.4 +/- 11.8 yrs.) who fulfilled criteria for fibromyalgia.</p> <p>Results</p> <p>Chronic post-SARS is characterized by persistent fatigue, diffuse myalgia, weakness, depression, and nonrestorative sleep with associated REM-related apneas/hypopneas, an elevated sleep EEG cyclical alternating pattern, and alpha EEG sleep anomaly. Post- SARS patients had symptoms of pre and post-sleep fatigue and post sleep sleepiness that were similar to the symptoms of patients with FMS, and similar to symptoms of patients with chronic fatigue syndrome. Both post-SARS and FMS groups had sleep instability as indicated by the high sleep EEG cyclical alternating pattern rate. The post-SARS group had a lower rating of the alpha EEG sleep anomaly as compared to the FMS patients. The post-SARS group also reported less pre-sleep and post-sleep musculoskeletal pain symptoms.</p> <p>Conclusions</p> <p>The clinical and sleep features of chronic post-SARS form a syndrome of chronic fatigue, pain, weakness, depression and sleep disturbance, which overlaps with the clinical and sleep features of FMS and chronic fatigue syndrome.</p
Probing SUSY CP Violation in Two-Body Stop Decays at the LHC
We study CP asymmetries in two-body decays of top squarks into neutralinos
and sleptons at the LHC. These asymmetries are used to probe the CP phases
possibly present in the stop and neutralino sector of the Minimal
Supersymmetric Standard Model. Taking into account bounds from experimental
electric dipole moment searches, we identify areas in the mSUGRA parameter
space where CP asymmetries can be sizeable and discuss the feasibility of their
observation at the LHC. As a result, potentially detectable CP asymmetries in
stop decays at the LHC are found, motivating further detailed experimental
studies for probing SUSY CP phases.Comment: 38 pages, 13 figures, error in Yukawa coupling corrected, revised
benchmark scenario and figures, JHEP versio
Integração e continuidade do cuidado em modelos de rede de atenção Ă saĂșde para idosos frĂĄgeis
Comparison of clinical rating scales in genetic frontotemporal dementia within the GENFI cohort
BACKGROUND: Therapeutic trials are now underway in genetic forms of frontotemporal dementia (FTD) but clinical outcome measures are limited. The two most commonly used measures, the Clinical Dementia Rating (CDR)+National Alzheimerâs Disease Coordinating Center (NACC)âFrontotemporal Lobar Degeneration (FTLD) and the FTD Rating Scale (FRS), have yet to be compared in detail in the genetic forms of FTD. METHODS: The CDR+NACCâFTLD and FRS were assessed cross-sectionally in 725 consecutively recruited participants from the Genetic FTD Initiative: 457 mutation carriers (77 microtubule-associated protein tau (MAPT), 187 GRN, 193 C9orf72) and 268 family members without mutations (non-carrier control group). 231 mutation carriers (51 MAPT, 92 GRN, 88 C9orf72) and 145 non-carriers had available longitudinal data at a follow-up time point. RESULTS: Cross-sectionally, the mean FRS score was lower in all genetic groups compared with controls: GRN mutation carriers mean 83.4 (SD 27.0), MAPT mutation carriers 78.2 (28.8), C9orf72 mutation carriers 71.0 (34.0), controls 96.2 (7.7), p<0.001 for all comparisons, while the mean CDR+NACCâFTLD Sum of Boxes was significantly higher in all genetic groups: GRN mutation carriers mean 2.6 (5.2), MAPT mutation carriers 3.2 (5.6), C9orf72 mutation carriers 4.2 (6.2), controls 0.2 (0.6), p<0.001 for all comparisons. Mean FRS score decreased and CDR+NACCâFTLD Sum of Boxes increased with increasing disease severity within each individual genetic group. FRS and CDR+NACCâFTLD Sum of Boxes scores were strongly negatively correlated across all mutation carriers (r_{s} =â0.77, p<0.001) and within each genetic group (r_{s} =â0.67âto â0.81, p<0.001 in each group). Nonetheless, discrepancies in disease staging were seen between the scales, and with each scale and clinician-judged symptomatic status. Longitudinally, annualised change in both FRS and CDR+NACCâFTLD Sum of Boxes scores initially increased with disease severity level before decreasing in those with the most severe disease: controls â0.1 (6.0) for FRS, â0.1 (0.4) for CDR+NACCâFTLD Sum of Boxes, asymptomatic mutation carriers â0.5 (8.2), 0.2 (0.9), prodromal disease â2.3 (9.9), 0.6 (2.7), mild disease â10.2 (18.6), 3.0 (4.1), moderate disease â9.6 (16.6), 4.4 (4.0), severe disease â2.7 (8.3), 1.7 (3.3). Sample sizes were calculated for a trial of prodromal mutation carriers: over 180 participants per arm would be needed to detect a moderate sized effect (30%) for both outcome measures, with sample sizes lower for the FRS. CONCLUSIONS: Both the FRS and CDR+NACCâFTLD measure disease severity in genetic FTD mutation carriers throughout the timeline of their disease, although the FRS may be preferable as an outcome measure. However, neither address a number of key symptoms in the FTD spectrum, for example, motor and neuropsychiatric deficits, which future scales will need to incorporate
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A data-driven disease progression model of fluid biomarkers in genetic frontotemporal dementia
Supplementary material: Supplementary material is available at Brain online: https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/brain/145/5/10.1093_brain_awab382/1/awab382_supplementary_data.zip?Expires=1665139578&Signature=C7VStQxldRqnpcchAWh4igaKwveciF~gaQCbInqMnI1YkIFV0euPXlI-0ZlRZ26hbRum6myjm88d3KzOM-wqVG~H7JO9TTUXoyi-n3hRRd1a4Vw0Hay9ykagca92gMqWij5ax4WzsEGlv~dKGSKKivH02pflzQyDAwF6xjjObYRYe29grdOZQ5h8orT6XNAdK5YFqpiX7L6mpVaNs7AOgNDdxtwshaa4kq1xxCgojTgAaIR3WFTFDpHkJ6wnhncxuteykTzq5~w1RCoDIfKQSA9C42i~iWryOeOvjv-P6j-R0tSkDGzFKcI3kUo3lUT9GiPG-vDwAO5EsLkUikJLOw__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA.GENFI consortium members
Full details are available in the Supplementary material.
SĂłnia Afonso, Maria Rosario Almeida, Sarah Anderl-Straub, Christin Andersson, Anna Antonell, Silvana Archetti, Andrea Arighi, Mircea Balasa, Myriam Barandiaran, Nuria BargallĂł, Robart Bartha, Benjamin Bender, Alberto Benussi, Luisa Benussi, Valentina Bessi, Giuliano Binetti, Sandra Black, Martina Bocchetta, Sergi Borrego-Ecija, Jose Bras, Rose Bruffaerts, Marta Cañada, Valentina Cantoni, Paola Caroppo, David Cash, Miguel Castelo-Branco, Rhian Convery, Thomas Cope, Giuseppe Di Fede, Alina DĂez, Diana Duro, Chiara Fenoglio, Camilla Ferrari, Catarina B. Ferreira, Nick Fox, Morris Freedman, Giorgio Fumagalli, Alazne Gabilondo, Roberto Gasparotti, Serge Gauthier, Stefano Gazzina, Giorgio Giaccone, Ana Gorostidi, Caroline Greaves, Rita Guerreiro, Tobias Hoegen, Begoña Indakoetxea, Vesna Jelic, Hans-Otto Karnath, Ron Keren, Tobias Langheinrich, Maria JoĂŁo LeitĂŁo, Albert LladĂł, Gemma Lombardi, Sandra Loosli, Carolina Maruta, Simon Mead, Gabriel Miltenberger, Rick van Minkelen, Sara Mitchell, Katrina Moore, Benedetta Nacmias, Jennifer Nicholas, Linn Ăijerstedt, Jaume Olives, Sebastien Ourselin, Alessandro Padovani, Georgia Peakman, Michela Pievani, Yolande Pijnenburg, Cristina Polito, Enrico Premi, Sara Prioni, Catharina Prix, Rosa Rademakers, Veronica Redaelli, Tim Rittman, Ekaterina Rogaeva, Pedro Rosa-Neto, Giacomina Rossi, Martin Rosser, Beatriz Santiago, Elio Scarpini, Sonja Schönecker, Elisa Semler, Rachelle Shafei, Christen Shoesmith, Miguel TĂĄbuas-Pereira, Mikel Tainta, Ricardo Taipa, David Tang-Wai, David L Thomas, Paul Thompson, Hakan Thonberg, Carolyn Timberlake, Pietro Tiraboschi, Emily Todd, Philip Van Damme, Mathieu Vandenbulcke, Michele Veldsman, Ana Verdelho, Jorge Villanua, Jason Warren, Ione Woollacott, Elisabeth Wlasich, Miren Zulaica.Copyright © The Author(s) 2021. Several CSF and blood biomarkers for genetic frontotemporal dementia have been proposed, including those reflecting neuroaxonal loss (neurofilament light chain and phosphorylated neurofilament heavy chain), synapse dysfunction [neuronal pentraxin 2 (NPTX2)], astrogliosis (glial fibrillary acidic protein) and complement activation (C1q, C3b). Determining the sequence in which biomarkers become abnormal over the course of disease could facilitate disease staging and help identify mutation carriers with prodromal or early-stage frontotemporal dementia, which is especially important as pharmaceutical trials emerge. We aimed to model the sequence of biomarker abnormalities in presymptomatic and symptomatic genetic frontotemporal dementia using cross-sectional data from the Genetic Frontotemporal dementia Initiative (GENFI), a longitudinal cohort study. Two-hundred and seventy-five presymptomatic and 127 symptomatic carriers of mutations in GRN, C9orf72 or MAPT, as well as 247 non-carriers, were selected from the GENFI cohort based on availability of one or more of the aforementioned biomarkers. Nine presymptomatic carriers developed symptoms within 18 months of sample collection ('converters'). Sequences of biomarker abnormalities were modelled for the entire group using discriminative event-based modelling (DEBM) and for each genetic subgroup using co-initialized DEBM. These models estimate probabilistic biomarker abnormalities in a data-driven way and do not rely on previous diagnostic information or biomarker cut-off points. Using cross-validation, subjects were subsequently assigned a disease stage based on their position along the disease progression timeline. CSF NPTX2 was the first biomarker to become abnormal, followed by blood and CSF neurofilament light chain, blood phosphorylated neurofilament heavy chain, blood glial fibrillary acidic protein and finally CSF C3b and C1q. Biomarker orderings did not differ significantly between genetic subgroups, but more uncertainty was noted in the C9orf72 and MAPT groups than for GRN. Estimated disease stages could distinguish symptomatic from presymptomatic carriers and non-carriers with areas under the curve of 0.84 (95% confidence interval 0.80-0.89) and 0.90 (0.86-0.94) respectively. The areas under the curve to distinguish converters from non-converting presymptomatic carriers was 0.85 (0.75-0.95). Our data-driven model of genetic frontotemporal dementia revealed that NPTX2 and neurofilament light chain are the earliest to change among the selected biomarkers. Further research should investigate their utility as candidate selection tools for pharmaceutical trials. The model's ability to accurately estimate individual disease stages could improve patient stratification and track the efficacy of therapeutic interventions.Deltaplan Dementie (The Netherlands Organisation
for Health Research and Development and Alzheimer Nederland;
grant numbers 733050813,733050103 and 733050513), the Bluefield
Project to Cure Frontotemporal Dementia, the Dioraphte founda tion (grant number 1402 1300), the European Joint Programmeâ
Neurodegenerative Disease Research and the Netherlands
Organisation for Health Research and Development (PreFrontALS:
733051042, RiMod-FTD: 733051024); V.V. and S.K. have received
funding from the European Unionâs Horizon 2020 research and in novation programme under grant agreement no. 666992
(EuroPOND). E.B. was supported by the Hartstichting (PPP
Allowance, 2018B011); in Belgium by the Mady Browaeys Fonds
voor Onderzoek naar Frontotemporale Degeneratie; in the UK by
the MRC UK GENFI grant (MR/M023664/1); J.D.R. is supported by an
MRC Clinician Scientist Fellowship (MR/M008525/1) and has
received funding from the NIHR Rare Disease Translational
Research Collaboration (BRC149/NS/MH); I.J.S. is supported by the
Alzheimerâs Association; J.B.R. is supported by the Wellcome Trust
(103838); in Spain by the FundacioÂŽ MaratoÂŽ de TV3 (20143810 to
R.S.V.); in Germany by the Deutsche Forschungsgemeinschaft
(DFG, German Research Foundation) under Germanyâs Excellence
Strategy within the framework of the Munich Cluster for Systems
Neurology (EXC 2145 SyNergyâID 390857198) and by grant 779357
âSolve-RDâ from the Horizon 2020 Research and Innovation
Programme (to MS); in Sweden by grants from the Swedish FTD
Initiative funded by the Schošrling Foundation, grants from JPND
PreFrontALS Swedish Research Council (VR) 529â2014-7504,
Swedish Research Council (VR) 2015â02926, Swedish Research
Council (VR) 2018â02754, Swedish Brain Foundation, Swedish
Alzheimer Foundation, Stockholm County Council ALF, Swedish
Demensfonden, Stohnes foundation, Gamla Tjašnarinnor,
Karolinska Institutet Doctoral Funding and StratNeuro. H.Z. is a
Wallenberg Scholar
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