Renormalization Group Functions of the \phi^4 Theory in the Strong Coupling Limit: Analytical Results

The previous attempts of reconstructing the Gell-Mann-Low function \beta(g) of the \phi^4 theory by summing perturbation series give the asymptotic behavior \beta(g) = \beta_\infty g^\alpha in the limit g\to \infty, where \alpha \approx 1 for the space dimensions d = 2,3,4. It can be hypothesized that the asymptotic behavior is \beta(g) ~ g for all values of d. The consideration of the zero-dimensional case supports this hypothesis and reveals the mechanism of its appearance: it is associated with a zero of one of the functional integrals. The generalization of the analysis confirms the asymptotic behavior \beta(g)=\beta_\infty g in the general d-dimensional case. The asymptotic behavior of other renormalization group functions is constant. The connection with the zero-charge problem and triviality of the \phi^4 theory is discussed.Comment: PDF, 17 page

Summing Divergent Perturbative Series in a Strong Coupling Limit. The Gell-Mann - Low Function of the \phi^4 Theory

An algorithm is proposed for determining asymptotics of the sum of a perturbative series in the strong coupling limit using given values of the expansion coefficients. Operation of the algorithm is illustrated by test examples, method for estimating errors is developed, and an optimization procedure is described. Application of the algorithm to the $\phi^4$ theory gives a behavior $\beta(g)\approx 7.4 g^{0.96}$ at large $g$ for its Gell-Mann -- Low function. The fact that the exponent is close to unity can be interpreted as a manifestation of the logarithmic branching of the type $\beta(g)\sim g (\ln g)^{-\gamma}$ (with $\gamma\approx 0.14$), which is confirmed by independent evidence. In any case, the $\phi^4$ theory is internally consistent. The procedure of summing perturbartive series with arbitrary values of expansion parameter is discussed.Comment: 23 pages, PD

The Extragalactic Distance Scale Key Project XXVII. A Derivation of the Hubble Constant Using the Fundamental Plane and Dn-Sigma Relations in Leo I, Virgo, and Fornax

Using published photometry and spectroscopy, we construct the fundamental plane and D_n-Sigma relations in Leo I, Virgo and Fornax. The published Cepheid P-L relations to spirals in these clusters fixes the relation between angular size and metric distance for both the fundamental plane and D_n-Sigma relations. Using the locally calibrated fundamental plane, we infer distances to a sample of clusters with a mean redshift of cz \approx 6000 \kms, and derive a value of H_0=78+- 5+- 9 km/s/Mpc (random, systematic) for the local expansion rate. This value includes a correction for depth effects in the Cepheid distances to the nearby clusters, which decreased the deduced value of the expansion rate by 5% +- 5%. If one further adopts the metallicity correction to the Cepheid PL relation, as derived by the Key Project, the value of the Hubble constant would decrease by a further 6%+- 4%. These two sources of systematic error, when combined with a +- 6% error due to the uncertainty in the distance to the Large Magellanic Cloud, a +- 4% error due to uncertainties in the WFPC2 calibration, and several small sources of uncertainty in the fundamental plane analysis, combine to yield a total systematic uncertainty of +- 11%. We find that the values obtained using either the CMB, or a flow-field model, for the reference frame of the distant clusters, agree to within 1%. The Dn-Sigma relation also produces similar results, as expected from the correlated nature of the two scaling relations. A complete discussion of the sources of random and systematic error in this determination of the Hubble constant is also given, in order to facilitate comparison with the other secondary indicators being used by the Key Project.Comment: 21 pages, 3 figures, Accepted for publication in Ap

Minor-axis velocity gradients in spirals and the case of inner polar disks

We measured the ionized-gas and stellar kinematics along the major and minor axis of a sample of 10 early-type spirals. Much to our surprise we found a remarkable gas velocity gradient along the minor axis of 8 of them. According to the kinematic features observed in their ionized-gas velocity fields, we divide our sample galaxies in three classes of objects. (i) NGC 4984, NGC 7213, and NGC 7377 show an overall velocity curve along the minor axis without zero-velocity points, out to the last measured radius, which is interpreted as due to the warped structure of the gaseous disk. (ii) NGC 3885, NGC 4224, and NGC 4586 are characterized by a velocity gradient along both major and minor axis, although non-zero velocities along the minor axis are confined to the central regions. Such gas kinematics have been explained as being due to non-circular motions induced by a triaxial potential. (iii) NGC 2855 and NGC 7049 show a change of slope of the velocity gradient measured along the major axis (which is shallower in the center and steeper away from the nucleus), as well as non-zero gas velocities in the central regions of the minor axis. This has been attributed to the presence of a kinematically-decoupled gaseous component in orthogonal rotation with respect to the galaxy disk, namely an inner polar disk. The case and origin of inner polar disks are discussed and the list of their host galaxies is presented.Comment: 13 pages. 3 PostScript figures (Figs. 1 and 3 at lower resolution). Accepted for publication in A&

Kinematic properties of early-type galaxy haloes using planetary nebulae

We present new planetary nebulae (PNe) positions, radial velocities, and magnitudes for 6 early-type galaxies obtained with the Planetary Nebulae Spectrograph, their two-dimensional velocity and velocity dispersion fields. We extend this study to include an additional 10 early-type galaxies with PNe radial velocity measurements available from the literature, to obtain a broader description of the outer-halo kinematics in early-type galaxies. These data extend the information derived from stellar kinematics to typically up to ~8 Re. The combination of photometry, stellar and PNe kinematics shows: i) good agreement between the PNe number density and the stellar surface brightness in the region where the two data sets overlap; ii) good agreement between PNe and stellar kinematics; iii) that the mean rms velocity profiles fall into two groups: with of the galaxies characterized by slowly decreasing profiles and the remainder having steeply falling profiles; iv) a larger variety of velocity dispersion profiles; v) that twists and misalignments in the velocity fields are more frequent at large radii, including some fast rotators; vi) that outer haloes are characterised by more complex radial profiles of the specific angular momentum-related lambda_R parameter than observed within 1Re; vii) that many objects are more rotationally dominated at large radii than in their central parts; and viii) that the halo kinematics are correlated with other galaxy properties, such as total luminosity, isophotal shape, total stellar mass, V/sigma, and alpha parameter, with a clear separation between fast and slow rotators.Comment: 36 pages, 21 figures, revised version for MNRA

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 Alzheimer’s Disease Coordinating Center (NACC) Frontotemporal 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+NACC FTLD 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+NACC FTLD 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+NACC FTLD Sum of Boxes increased with increasing disease severity within each individual genetic group. FRS and CDR+NACC FTLD Sum of Boxes scores were strongly negatively correlated across all mutation carriers (r_{s} =−0.77, p<0.001) and within each genetic group (r_{s} =−0.67 to −0.81, 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+NACC FTLD Sum of Boxes scores initially increased with disease severity level before decreasing in those with the most severe disease: controls −0.1 (6.0) for FRS, −0.1 (0.4) for CDR+NACC FTLD Sum of Boxes, asymptomatic mutation carriers −0.5 (8.2), 0.2 (0.9), prodromal disease −2.3 (9.9), 0.6 (2.7), mild disease −10.2 (18.6), 3.0 (4.1), moderate disease −9.6 (16.6), 4.4 (4.0), severe disease −2.7 (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+NACC FTLD 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

Human resources for maternal health: multi-purpose or specialists?

A crucial question in the aim to attain MDG5 is whether it can be achieved faster with the scaling up of multi-purpose health workers operating in the community or with the scaling up of professional skilled birth attendants working in health facilities. Most advisers concerned with maternal mortality reduction concur to promote births in facilities with professional attendants as the ultimate strategy. The evidence, however, is scarce on what it takes to progress in this path, and on the 'interim solutions' for situations where the majority of women still deliver at home. These questions are particularly relevant as we have reached the twentieth anniversary of the safe motherhood initiative without much progress made

Timing of HPV16-E6 antibody seroconversion before OPSCC : findings from the HPVC3 consortium

Background: Human papillomavirus type 16 (HPV16)-E6 antibodies are detectable in peripheral blood before diagnosis in the majority of HPV16-driven oropharyngeal squamous cell carcinoma (OPSCC), but the timing of seroconversion is unknown. Patients and methods: We formed the HPV Cancer Cohort Consortium which comprises nine population cohorts from Europe, North America and Australia. In total, 743 incident OPSCC cases and 5814 controls provided at least one pre-diagnostic blood sample, including 111 cases with multiple samples. Median time between first blood collection and OPSCC diagnosis was 11.4 years (IQR = 6-11 years, range = 0-40 years). Antibodies against HPV16-E6 were measured by multiplex serology (GST fusion protein based Luminex assay). Results: HPV16-E6 seropositivity was present in 0.4% of controls (22/5814; 95% CI 0.2% to 0.6%) and 26.2% (195/743; 95% CI 23.1% to 29.6%) of OPSCC cases. HPV16-E6 seropositivity increased the odds of OPSCC 98.2-fold (95% CI 62.1-155.4) in whites and 17.2-fold (95% CI 1.7-170.5) in blacks. Seropositivity in cases was more frequent in recent calendar periods, ranging from 21.9% pre-1996 to 68.4% in 2005 onwards, in those with blood collection near diagnosis (lead time 30 years (N = 24), 20-30 years (N = 148), 10-20 years (N = 228), and Conclusions: The immune response to HPV16-driven tumorigenesis is most often detectable several decades before OPSCC diagnosis. HPV16-E6 seropositive individuals face increased risk of OPSCC over several decades.Peer reviewe

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. Sónia Afonso, Maria Rosario Almeida, Sarah Anderl-Straub, Christin Andersson, Anna Antonell, Silvana Archetti, Andrea Arighi, Mircea Balasa, Myriam Barandiaran, Nuria Bargalló, 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 Díez, 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 João Leitão, Albert Lladó, Gemma Lombardi, Sandra Loosli, Carolina Maruta, Simon Mead, Gabriel Miltenberger, Rick van Minkelen, Sara Mitchell, Katrina Moore, Benedetta Nacmias, Jennifer Nicholas, Linn Öijerstedt, 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 Tábuas-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 Programme— 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 Union’s 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 Alzheimer’s Association; J.B.R. is supported by the Wellcome Trust (103838); in Spain by the Fundacio´ Marato´ de TV3 (20143810 to R.S.V.); in Germany by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy—ID 390857198) and by grant 779357 ‘Solve-RD’ from the Horizon 2020 Research and Innovation Programme (to MS); in Sweden by grants from the Swedish FTD Initiative funded by the Scho¨rling Foundation, grants from JPND PreFrontALS Swedish Research Council (VR) 529–2014-7504, Swedish Research Council (VR) 2015–02926, Swedish Research Council (VR) 2018–02754, Swedish Brain Foundation, Swedish Alzheimer Foundation, Stockholm County Council ALF, Swedish Demensfonden, Stohnes foundation, Gamla Tja¨narinnor, Karolinska Institutet Doctoral Funding and StratNeuro. H.Z. is a Wallenberg Scholar

Physics of Neutron Star Crusts

The physics of neutron star crusts is vast, involving many different research fields, from nuclear and condensed matter physics to general relativity. This review summarizes the progress, which has been achieved over the last few years, in modeling neutron star crusts, both at the microscopic and macroscopic levels. The confrontation of these theoretical models with observations is also briefly discussed.Comment: 182 pages, published version available at <http://www.livingreviews.org/lrr-2008-10