On the shape of a D-brane bound state and its topology change

As is well known, coordinates of D-branes are described by NxN matrices. From generic non-commuting matrices, it is difficult to extract physics, for example, the shape of the distribution of positions of D-branes. To overcome this problem, we generalize and elaborate on a simple prescription, first introduced by Hotta, Nishimura and Tsuchiya, which determines the most appropriate gauge to make the separation between diagonal components (D-brane positions) and off-diagonal components. This prescription makes it possible to extract the distribution of D-branes directly from matrices. We verify the power of it by applying it to Monte-Carlo simulations for various lower dimensional Yang-Mills matrix models. In particular, we detect the topology change of the D-brane bound state for a phase transition of a matrix model; the existence of this phase transition is expected from the gauge/gravity duality, and the pattern of the topology change is strikingly similar to the counterpart in the gravity side, the black hole/black string transition. We also propose a criterion, based on the behavior of the off-diagonal components, which determines when our prescription gives a sensible definition of D-brane positions. We provide numerical evidence that our criterion is satisfied for the typical distance between D-branes. For a supersymmetric model, positions of D-branes can be defined even at a shorter distance scale. The behavior of off-diagonal elements found in this analysis gives some support for previous studies of D-brane bound states.Comment: 29 pages, 16 figure

High temperature expansion in supersymmetric matrix quantum mechanics

We formulate the high temperature expansion in supersymmetric matrix quantum mechanics with 4, 8 and 16 supercharges. The models can be obtained by dimensionally reducing N=1 U(N) super Yang-Mills theory in D=4,6,10 to 1 dimension, respectively. While the non-zero frequency modes become weakly coupled at high temperature, the zero modes remain strongly coupled. We find, however, that the integration over the zero modes that remains after integrating out all the non-zero modes perturbatively, reduces to the evaluation of connected Green's functions in the bosonic IKKT model. We perform Monte Carlo simulation to compute these Green's functions, which are then used to obtain the coefficients of the high temperature expansion for various quantities up to the next-leading order. Our results nicely reproduce the asymptotic behaviors of the recent simulation results at finite temperature. In particular, the fermionic matrices, which decouple at the leading order, give rise to substantial effects at the next-leading order, reflecting finite temperature behaviors qualitatively different from the corresponding models without fermions.Comment: 17 pages, 13 figures, (v2) some typos correcte

Variation in experiences of nature across gradients of tree cover in compact and sprawling cities

Urban environments are expanding globally, and by 2050 nearly 70% of the world’s population will live in towns and cities, where opportunities to experience nature are more limited than in rural areas. This transition could have important implications for health and wellbeing given the diversity of benefits that nature delivers. Despite these issues, there is a lack of information on whether or how the experience of nature changes as green space becomes less available. We explore this question for residents of two case study cities of varying urban designs, sprawling (Brisbane, Australia) and compact (three English towns, U.K). Second, we examine how people’s feelings of connection to nature (measured using the Nature Relatedness scale) vary across this same gradient of nature availability. Despite climatic and cultural differences we found substantial similarities between the two locations. Lower levels of neighbourhood tree cover were associated with a reduced frequency of visits to private and public green spaces, and a similar pattern was found for the duration of time spent in private and public green spaces for Brisbane. Residents of both urban areas showed similar levels of nature relatedness, and there was a weak but positive association between tree cover and Nature Relatedness. These results suggest that regardless of the style of urban design, maintaining the availability of nature close to home is a critical step to protect people’s experiences of nature and their desire to seek out those experiences.D.F.S. is supported through ARC Discovery Grant DP120102857 and the Centre of Excellence for Environmental Decisions (CEED, Australia); R.A.F. holds an ARC Future Fellowship; D.T.C.C, S.H., K.A. and K.J.G. are supported by the Fragments, Functions, Flows and Urban Ecosystem Services project, NERC grant NE/J015237/1Connection to natureExtinction of experienceGreen spacesHuman well-beingNature relatednessUrban ecolog

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination

BACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript

Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials