Electron correlation effects in a wide channel from the ν=1\nu =1 quantum Hall edge states

The spatial behavior of Landau levels (LLs) for the $nu=1$ quantum Hall regime at the edge of a wide channel is studied in a self-consistent way by using a generalized local density approximation proposed here. Both exchange interaction and strong electron correlations, due to edge states, are taken into account. They essentially modify the spatial behavior of the occupied lowest spin-up LL in comparison with that of the lowest spin-down LL, which is totally empty. The contrast in the spatial behavior can be attributed to a different effective one-electron lateral confining potentials for the spin-split LLs. Many-body effects on the spatially inhomogeneous spin-splitting are calculated within the screened Hartree-Fock approximation. It is shown that, far from the edges, the maximum activation energy is dominated by the gap between the Fermi level and the bottom of the spin-down LL, because the gap between the Fermi level and the spin-up LL is much larger. In other words, the maximum activation energy in the bulk of the channel corresponds to a highly asymmetric position of the Fermi level within the gap between spin-down and spin-up LLs in the bulk. We have also studied the renormalization of the edge-state group velocity due to electron correlations. The results of the present theory are in line with those suggested and reported by experiments on high quality samples.Comment: 9 pages, 4 figure

A longitudinal study of impact and early stance loads during gait following arthroscopic partial meniscectomy

People following arthroscopic partial medial meniscectomy (APM) are at increased risk of developing knee osteoarthritis. High impact loading and peak loading early in the stance phase of gait may play a role in the pathogenesis of knee osteoarthritis. This was a secondary analysis of longitudinal data to investigate loading-related indices at baseline in an APM group (3 months post-surgery) and a healthy control group, and again 2 years later (follow-up). At baseline, 82 participants with medial APM and 38 healthy controls were assessed, with 66 and 23 re-assessed at follow-up, respectively. Outcome measures included: (i) heel strike transient (HST) presence and magnitude, (ii) maximum loading rate, (iii) peak vertical force (Fz) during early stance. At baseline, maximum loading rate was lower in the operated leg (APM) and non-operated leg (non-APM leg) compared to controls (p≤0.03) and peak Fz was lower in the APM leg compared to non-APM leg (p≤0.01). Over 2 years, peak Fz increased in the APM leg compared to the non-APM leg and controls (p≤0.01). Following recent APM, people may adapt their gait to protect the operated knee from excessive loads, as evidenced by a lower maximum loading rate in the APM leg compared to controls, and a reduced peak Fz in the APM leg compared to the non-APM leg. No differences at follow-up may suggest an eventual return to more typical gait. However, the increase in peak Fz in the APM leg may be of concern for long-term joint health given the compromised function of the meniscus

Mechanisms underpinning longitudinal increases in the knee adduction moment following arthroscopic partial meniscectomy

Background Knee osteoarthritis is common following arthroscopic partial meniscectomy and a higher external peak knee adduction moment is believed to be a contributor. The peak knee adduction moment has been shown to increase over 2 years (from 3-months post-arthroscopic partial meniscectomy). The aim of this study was to evaluate mechanisms underpinning the increase in peak knee adduction moment over 2 years observed in people 3-months following arthroscopic partial meniscectomy. Methods Sixty-six participants with medial arthroscopic partial meniscectomy were assessed at baseline and again 2 years later. Parameters were evaluated at time of peak knee adduction moment as participants walked barefoot at their self-selected normal and fast pace for both time points. Findings For normal pace walking, an increase in frontal plane ground reaction force-to-knee lever arm accounted for 30% of the increase in peak knee adduction moment (B = 0.806 [95% CI 0.501–1.110], P < 0.001). For fast pace walking, an increase in the frontal plane ground reaction force magnitude accounted for 21% of the increase in peak knee adduction moment (B = 2.343 [95% CI 1.219–3.468], P < 0.001); with an increase in tibia varus angle accounting for a further 15% (B = 0.310 [95% CI 0.145–0.474], P < 0.001). Interpretation Our data suggest that an increase in lever arm and increase in frontal plane ground reaction force magnitude are contributors to the increased knee adduction moment observed over time in people following arthroscopic partial meniscectomy

Contemporary presence of dynamical and statistical production of intermediate mass fragments in midperipheral 58^{58}Ni+58^{58}Ni collisions at 30 MeV/nucleon

The $^{58}Ni+^{58}Ni$ reaction at 30 MeV/nucleon has been experimentally investigated at the Superconducting Cyclotron of the INFN Laboratori Nazionali del Sud. In midperipheral collisions the production of massive fragments (4$\le$Z$\le$12), consistent with the statistical fragmentation of the projectile-like residue and the dynamical formation of a neck, joining projectile-like and target-like residues, has been observed. The fragments coming from these different processes differ both in charge distribution and isotopic composition. In particular it is shown that these mechanisms leading to fragment production act contemporarily inside the same event.Comment: 9 pages, minor correction

Size and asymmetry of the reaction entrance channel: influence on the probability of neck production

The results of experiments performed to investigate the Ni+Al, Ni+Ni, Ni+Ag reactions at 30 MeV/nucleon are presented. From the study of dissipative midperipheral collisions, it has been possible to detect events in which Intermediate Mass Fragments (IMF) production takes place. The decay of a quasi-projectile has been identified; its excitation energy leads to a multifragmentation totally described in terms of a statistical disassembly of a thermalized system (T$\simeq$4 MeV, E$^*\simeq$4 MeV/nucleon). Moreover, for the systems Ni+Ni, Ni+Ag, in the same nuclear reaction, a source with velocity intermediate between that of the quasi-projectile and that of the quasi-target, emitting IMF, is observed. The fragments produced by this source are more neutron rich than the average matter of the overall system, and have a charge distribution different, with respect to those statistically emitted from the quasi-projectile. The above features can be considered as a signature of the dynamical origin of the midvelocity emission. The results of this analysis show that IMF can be produced via different mechanisms simultaneously present within the same collision. Moreover, once fixed the characteristics of the quasi-projectile in the three considered reactions (in size, excitation energy and temperature), one observes that the probability of a partner IMF production via dynamical mechanism has a threshold (not present in the Ni+Al case) and increases with the size of the target nucleus.Comment: 16 pages, 7 figures, accepted for publication on Nuclear Physics

Fragment Isospin as a Probe of Heavy-Ion Collisions

Isotope ratios of fragments produced at mid-rapidity in peripheral and central collisions of 114Cd ions with 92Mo and 98Mo target nuclei at E/A = 50 MeV are compared. Neutron-rich isotopes are preferentially produced in central collisions as compared to peripheral collisions. The influence of the size (A), density, N/Z, E*/A, and Eflow/A of the emitting source on the measured isotope ratios was explored by comparison with a statistical model (SMM). The mid-rapidity region associated with peripheral collisions does not appear to be neutron-enriched relative to central collisions.Comment: 12 pages including figure

Isospin influences on particle emission and critical phenomenon in nuclear dissociation

Features of particle emission and critical point behavior are investigated as functions of the isospin of disassembling sources and temperature at a moderate freeze-out density for medium-size Xe isotopes in the framework of isospin dependent lattice gas model. Multiplicities of emitted light particles, isotopic and isobaric ratios of light particles show the strong dependence on the isospin of the dissociation source, but double ratios of light isotope pairs and the critical temperature determined by the extreme values of some critical observables are insensitive to the isospin of the systems. Values of the power law parameter of cluster mass distribution, mean multiplicity of intermediate mass fragments ($IMF$), information entropy ($H$) and Campi's second moment ($S_2$) also show a minor dependence on the isospin of Xe isotopes at the critical point. In addition, the slopes of the average multiplicites of the neutrons ($N_n$), protons ($N_p$), charged particles ($N_{CP}$), and IMFs ($N_{imf}$), slopes of the largest fragment mass number ($A_{max}$), and the excitation energy per nucleon of the disassembling source ($E^*/A$) to temperature are investigated as well as variances of the distributions of $N_n$, $N_p$, $N_{CP}$, $N_{IMF}$, $A_{max}$ and $E^*/A$. It is found that they can be taken as additional judgements to the critical phenomena.Comment: 9 Pages, 8 figure

Primary stroke prevention worldwide : translating evidence into action

Funding Information: The stroke services survey reported in this publication was partly supported by World Stroke Organization and Auckland University of Technology. VLF was partly supported by the grants received from the Health Research Council of New Zealand. MOO was supported by the US National Institutes of Health (SIREN U54 HG007479) under the H3Africa initiative and SIBS Genomics (R01NS107900, R01NS107900-02S1, R01NS115944-01, 3U24HG009780-03S5, and 1R01NS114045-01), Sub-Saharan Africa Conference on Stroke Conference (1R13NS115395-01A1), and Training Africans to Lead and Execute Neurological Trials & Studies (D43TW012030). AGT was supported by the Australian National Health and Medical Research Council. SLG was supported by a National Heart Foundation of Australia Future Leader Fellowship and an Australian National Health and Medical Research Council synergy grant. We thank Anita Arsovska (University Clinic of Neurology, Skopje, North Macedonia), Manoj Bohara (HAMS Hospital, Kathmandu, Nepal), Denis ?erimagi? (Poliklinika Glavi?, Dubrovnik, Croatia), Manuel Correia (Hospital de Santo Ant?nio, Porto, Portugal), Daissy Liliana Mora Cuervo (Hospital Moinhos de Vento, Porto Alegre, Brazil), Anna Cz?onkowska (Institute of Psychiatry and Neurology, Warsaw, Poland), Gloria Ekeng (Stroke Care International, Dartford, UK), Jo?o Sargento-Freitas (Centro Hospitalar e Universit?rio de Coimbra, Coimbra, Portugal), Yuriy Flomin (MC Universal Clinic Oberig, Kyiv, Ukraine), Mehari Gebreyohanns (UT Southwestern Medical Centre, Dallas, TX, USA), Ivete Pillo Gon?alves (Hospital S?o Jos? do Avai, Itaperuna, Brazil), Claiborne Johnston (Dell Medical School, University of Texas, Austin, TX, USA), Kristaps Jurj?ns (P Stradins Clinical University Hospital, Riga, Latvia), Rizwan Kalani (University of Washington, Seattle, WA, USA), Grzegorz Kozera (Medical University of Gda?sk, Gda?sk, Poland), Kursad Kutluk (Dokuz Eylul University, ?zmir, Turkey), Branko Malojcic (University Hospital Centre Zagreb, Zagreb, Croatia), Micha? Maluchnik (Ministry of Health, Warsaw, Poland), Evija Migl?ne (P Stradins Clinical University Hospital, Riga, Latvia), Cassandra Ocampo (University of Botswana, Princess Marina Hospital, Botswana), Louise Shaw (Royal United Hospitals Bath NHS Foundation Trust, Bath, UK), Lekhjung Thapa (Upendra Devkota Memorial-National Institute of Neurological and Allied Sciences, Kathmandu, Nepal), Bogdan Wojtyniak (National Institute of Public Health, Warsaw, Poland), Jie Yang (First Affiliated Hospital of Chengdu Medical College, Chengdu, China), and Tomasz Zdrojewski (Medical University of Gda?sk, Gda?sk, Poland) for their comments on early draft of the manuscript. The views expressed in this article are solely the responsibility of the authors and they do not necessarily reflect the views, decisions, or policies of the institution with which they are affiliated. We thank WSO for funding. The funder had no role in the design, data collection, analysis and interpretation of the study results, writing of the report, or the decision to submit the study results for publication. Funding Information: The stroke services survey reported in this publication was partly supported by World Stroke Organization and Auckland University of Technology. VLF was partly supported by the grants received from the Health Research Council of New Zealand. MOO was supported by the US National Institutes of Health (SIREN U54 HG007479) under the H3Africa initiative and SIBS Genomics (R01NS107900, R01NS107900-02S1, R01NS115944-01, 3U24HG009780-03S5, and 1R01NS114045-01), Sub-Saharan Africa Conference on Stroke Conference (1R13NS115395-01A1), and Training Africans to Lead and Execute Neurological Trials & Studies (D43TW012030). AGT was supported by the Australian National Health and Medical Research Council. SLG was supported by a National Heart Foundation of Australia Future Leader Fellowship and an Australian National Health and Medical Research Council synergy grant. We thank Anita Arsovska (University Clinic of Neurology, Skopje, North Macedonia), Manoj Bohara (HAMS Hospital, Kathmandu, Nepal), Denis Čerimagić (Poliklinika Glavić, Dubrovnik, Croatia), Manuel Correia (Hospital de Santo António, Porto, Portugal), Daissy Liliana Mora Cuervo (Hospital Moinhos de Vento, Porto Alegre, Brazil), Anna Członkowska (Institute of Psychiatry and Neurology, Warsaw, Poland), Gloria Ekeng (Stroke Care International, Dartford, UK), João Sargento-Freitas (Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal), Yuriy Flomin (MC Universal Clinic Oberig, Kyiv, Ukraine), Mehari Gebreyohanns (UT Southwestern Medical Centre, Dallas, TX, USA), Ivete Pillo Gonçalves (Hospital São José do Avai, Itaperuna, Brazil), Claiborne Johnston (Dell Medical School, University of Texas, Austin, TX, USA), Kristaps Jurjāns (P Stradins Clinical University Hospital, Riga, Latvia), Rizwan Kalani (University of Washington, Seattle, WA, USA), Grzegorz Kozera (Medical University of Gdańsk, Gdańsk, Poland), Kursad Kutluk (Dokuz Eylul University, İzmir, Turkey), Branko Malojcic (University Hospital Centre Zagreb, Zagreb, Croatia), Michał Maluchnik (Ministry of Health, Warsaw, Poland), Evija Miglāne (P Stradins Clinical University Hospital, Riga, Latvia), Cassandra Ocampo (University of Botswana, Princess Marina Hospital, Botswana), Louise Shaw (Royal United Hospitals Bath NHS Foundation Trust, Bath, UK), Lekhjung Thapa (Upendra Devkota Memorial-National Institute of Neurological and Allied Sciences, Kathmandu, Nepal), Bogdan Wojtyniak (National Institute of Public Health, Warsaw, Poland), Jie Yang (First Affiliated Hospital of Chengdu Medical College, Chengdu, China), and Tomasz Zdrojewski (Medical University of Gdańsk, Gdańsk, Poland) for their comments on early draft of the manuscript. The views expressed in this article are solely the responsibility of the authors and they do not necessarily reflect the views, decisions, or policies of the institution with which they are affiliated. We thank WSO for funding. The funder had no role in the design, data collection, analysis and interpretation of the study results, writing of the report, or the decision to submit the study results for publication. Funding Information: VLF declares that the PreventS web app and Stroke Riskometer app are owned and copyrighted by Auckland University of Technology; has received grants from the Brain Research New Zealand Centre of Research Excellence (16/STH/36), Australian National Health and Medical Research Council (NHMRC; APP1182071), and World Stroke Organization (WSO); is an executive committee member of WSO, honorary medical director of Stroke Central New Zealand, and CEO of New Zealand Stroke Education charitable Trust. AGT declares funding from NHMRC (GNT1042600, GNT1122455, GNT1171966, GNT1143155, and GNT1182017), Stroke Foundation Australia (SG1807), and Heart Foundation Australia (VG102282); and board membership of the Stroke Foundation (Australia). SLG is funded by the National Health Foundation of Australia (Future Leader Fellowship 102061) and NHMRC (GNT1182071, GNT1143155, and GNT1128373). RM is supported by the Implementation Research Network in Stroke Care Quality of the European Cooperation in Science and Technology (project CA18118) and by the IRIS-TEPUS project from the inter-excellence inter-cost programme of the Ministry of Education, Youth and Sports of the Czech Republic (project LTC20051). BN declares receiving fees for data management committee work for SOCRATES and THALES trials for AstraZeneca and fees for data management committee work for NAVIGATE-ESUS trial from Bayer. All other authors declare no competing interests. Publisher Copyright: © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseStroke is the second leading cause of death and the third leading cause of disability worldwide and its burden is increasing rapidly in low-income and middle-income countries, many of which are unable to face the challenges it imposes. In this Health Policy paper on primary stroke prevention, we provide an overview of the current situation regarding primary prevention services, estimate the cost of stroke and stroke prevention, and identify deficiencies in existing guidelines and gaps in primary prevention. We also offer a set of pragmatic solutions for implementation of primary stroke prevention, with an emphasis on the role of governments and population-wide strategies, including task-shifting and sharing and health system re-engineering. Implementation of primary stroke prevention involves patients, health professionals, funders, policy makers, implementation partners, and the entire population along the life course.publishersversionPeer reviewe