Pressure Gradients Driving Ion Transport in the Topside Martian Atmosphere

An edited version of this paper was published by AGU. Copyright 2019 American Geophysical Union.Magnetic and thermal pressure gradient forces drive plasma flow in the topside ionosphere of Mars. Some of this flow can contribute to ion loss from the planet and thus affect atmospheric evolution. MAVEN measurements of the magnetic field, electron density, and electron temperature, taken over a 3‐year time period, are used to obtain averaged magnetic and thermal pressures in the topside ionosphere versus altitude, solar zenith angle, and latitude. Magnetic pressures are several times greater than thermal pressures for altitudes greater than about 300 km; that is, the plasma beta is less than one. The total pressure increases with altitude in the ionosphere and decreases with increasing solar zenith angle. Using these pressure patterns in the dayside ionosphere to estimate the pressure gradient force in the fluid momentum equation, we estimate horizontal day‐to‐night plasma flow speeds of a few kilometers per second near 400 km

Estimates of Ionospheric Transport and Ion Loss at Mars

Ion loss from the topside ionosphere of Mars associated with the solar wind interaction makes an important contribution to the loss of volatiles from this planet. Data from NASA's Mars Atmosphere and Volatile Evolution mission combined with theoretical modeling are now helping us to understand the processes involved in the ion loss process. Given the complexity of the solar wind interaction, motivation exists for considering a simple approach to this problem and for understanding how the loss rates might scale with solar wind conditions and solar extreme ultraviolet irradiance. This paper reviews the processes involved in the ionospheric dynamics. Simple analytical and semiempirical expressions for ion flow speeds and ion loss are derived. In agreement with more sophisticated models and with purely empirical studies, it is found that the oxygen loss rate from ion transport is about 5% (i.e., global O ion loss rate of Qion ≈ 4 × 1024 s−1) of the total oxygen loss rate. The ion loss is found to approximately scale as the square root of the solar ionizing photon flux and also as the square root of the solar wind dynamic pressure. Typical ion flow speeds are found to be about 1 km/s in the topside ionosphere near an altitude of 300 km on the dayside. Not surprisingly, the plasma flow speed is found to increase with altitude due to the decreasing ion‐neutral collision frequency

Estimates of Ionospheric Transport and Ion Loss at Mars

Ion loss from the topside ionosphere of Mars associated with the solar wind interaction makes an important contribution to the loss of volatiles from this planet. Data from NASA’s Mars Atmosphere and Volatile Evolution mission combined with theoretical modeling are now helping us to understand the processes involved in the ion loss process. Given the complexity of the solar wind interaction, motivation exists for considering a simple approach to this problem and for understanding how the loss rates might scale with solar wind conditions and solar extreme ultraviolet irradiance. This paper reviews the processes involved in the ionospheric dynamics. Simple analytical and semiempirical expressions for ion flow speeds and ion loss are derived. In agreement with more sophisticated models and with purely empirical studies, it is found that the oxygen loss rate from ion transport is about 5% (i.e., global O ion loss rate of Qion ≈ 4 × 1024 s−1) of the total oxygen loss rate. The ion loss is found to approximately scale as the square root of the solar ionizing photon flux and also as the square root of the solar wind dynamic pressure. Typical ion flow speeds are found to be about 1 km/s in the topside ionosphere near an altitude of 300 km on the dayside. Not surprisingly, the plasma flow speed is found to increase with altitude due to the decreasing ion‐neutral collision frequency.Key PointsOxygen ion loss from the ionosphere of Mars is mainly driven by magnetic forces generated by the solar wind interactionGlobal ion loss from Mars scales approximately as the square root of both the upstream solar wind pressure and solar ionizing photon fluxIon flow speeds in the ionosphere increase with altitude and with solar wind pressurePeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140009/1/jgra53859.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/140009/2/jgra53859_am.pd

Financial doping and financial fair play in European Club football competitions

Addresses the emerging area of manipulation in professional sports by bringing a collection of original contributions together in one volume for the first time Provides an interdisciplinary approach, combining economic, business administrative and legal issues, that enables a complete overview for any scholar interested in the global economics of, and manipulation of sport, in general Presents contributions from world class scholars that are well known in their area

A novel formulation of inhaled sodium cromoglicate (PA101) in idiopathic pulmonary fibrosis and chronic cough: a randomised, double-blind, proof-of-concept, phase 2 trial

Background Cough can be a debilitating symptom of idiopathic pulmonary fibrosis (IPF) and is difficult to treat. PA101 is a novel formulation of sodium cromoglicate delivered via a high-efficiency eFlow nebuliser that achieves significantly higher drug deposition in the lung compared with the existing formulations. We aimed to test the efficacy and safety of inhaled PA101 in patients with IPF and chronic cough and, to explore the antitussive mechanism of PA101, patients with chronic idiopathic cough (CIC) were also studied. Methods This pilot, proof-of-concept study consisted of a randomised, double-blind, placebo-controlled trial in patients with IPF and chronic cough and a parallel study of similar design in patients with CIC. Participants with IPF and chronic cough recruited from seven centres in the UK and the Netherlands were randomly assigned (1:1, using a computer-generated randomisation schedule) by site staff to receive PA101 (40 mg) or matching placebo three times a day via oral inhalation for 2 weeks, followed by a 2 week washout, and then crossed over to the other arm. Study participants, investigators, study staff, and the sponsor were masked to group assignment until all participants had completed the study. The primary efficacy endpoint was change from baseline in objective daytime cough frequency (from 24 h acoustic recording, Leicester Cough Monitor). The primary efficacy analysis included all participants who received at least one dose of study drug and had at least one post-baseline efficacy measurement. Safety analysis included all those who took at least one dose of study drug. In the second cohort, participants with CIC were randomly assigned in a study across four centres with similar design and endpoints. The study was registered with ClinicalTrials.gov (NCT02412020) and the EU Clinical Trials Register (EudraCT Number 2014-004025-40) and both cohorts are closed to new participants. Findings Between Feb 13, 2015, and Feb 2, 2016, 24 participants with IPF were randomly assigned to treatment groups. 28 participants with CIC were enrolled during the same period and 27 received study treatment. In patients with IPF, PA101 reduced daytime cough frequency by 31·1% at day 14 compared with placebo; daytime cough frequency decreased from a mean 55 (SD 55) coughs per h at baseline to 39 (29) coughs per h at day 14 following treatment with PA101, versus 51 (37) coughs per h at baseline to 52 (40) cough per h following placebo treatment (ratio of least-squares [LS] means 0·67, 95% CI 0·48–0·94, p=0·0241). By contrast, no treatment benefit for PA101 was observed in the CIC cohort; mean reduction of daytime cough frequency at day 14 for PA101 adjusted for placebo was 6·2% (ratio of LS means 1·27, 0·78–2·06, p=0·31). PA101 was well tolerated in both cohorts. The incidence of adverse events was similar between PA101 and placebo treatments, most adverse events were mild in severity, and no severe adverse events or serious adverse events were reported. Interpretation This study suggests that the mechanism of cough in IPF might be disease specific. Inhaled PA101 could be a treatment option for chronic cough in patients with IPF and warrants further investigation

Determinants of recovery from post-COVID-19 dyspnoea: analysis of UK prospective cohorts of hospitalised COVID-19 patients and community-based controls

Background The risk factors for recovery from COVID-19 dyspnoea are poorly understood. We investigated determinants of recovery from dyspnoea in adults with COVID-19 and compared these to determinants of recovery from non-COVID-19 dyspnoea. Methods We used data from two prospective cohort studies: PHOSP-COVID (patients hospitalised between March 2020 and April 2021 with COVID-19) and COVIDENCE UK (community cohort studied over the same time period). PHOSP-COVID data were collected during hospitalisation and at 5-month and 1-year follow-up visits. COVIDENCE UK data were obtained through baseline and monthly online questionnaires. Dyspnoea was measured in both cohorts with the Medical Research Council Dyspnoea Scale. We used multivariable logistic regression to identify determinants associated with a reduction in dyspnoea between 5-month and 1-year follow-up. Findings We included 990 PHOSP-COVID and 3309 COVIDENCE UK participants. We observed higher odds of improvement between 5-month and 1-year follow-up among PHOSP-COVID participants who were younger (odds ratio 1.02 per year, 95% CI 1.01–1.03), male (1.54, 1.16–2.04), neither obese nor severely obese (1.82, 1.06–3.13 and 4.19, 2.14–8.19, respectively), had no pre-existing anxiety or depression (1.56, 1.09–2.22) or cardiovascular disease (1.33, 1.00–1.79), and shorter hospital admission (1.01 per day, 1.00–1.02). Similar associations were found in those recovering from non-COVID-19 dyspnoea, excluding age (and length of hospital admission). Interpretation Factors associated with dyspnoea recovery at 1-year post-discharge among patients hospitalised with COVID-19 were similar to those among community controls without COVID-19. Funding PHOSP-COVID is supported by a grant from the MRC-UK Research and Innovation and the Department of Health and Social Care through the National Institute for Health Research (NIHR) rapid response panel to tackle COVID-19. The views expressed in the publication are those of the author(s) and not necessarily those of the National Health Service (NHS), the NIHR or the Department of Health and Social Care. COVIDENCE UK is supported by the UK Research and Innovation, the National Institute for Health Research, and Barts Charity. The views expressed are those of the authors and not necessarily those of the funders

Post-acute COVID-19 neuropsychiatric symptoms are not associated with ongoing nervous system injury

A proportion of patients infected with severe acute respiratory syndrome coronavirus 2 experience a range of neuropsychiatric symptoms months after infection, including cognitive deficits, depression and anxiety. The mechanisms underpinning such symptoms remain elusive. Recent research has demonstrated that nervous system injury can occur during COVID-19. Whether ongoing neural injury in the months after COVID-19 accounts for the ongoing or emergent neuropsychiatric symptoms is unclear. Within a large prospective cohort study of adult survivors who were hospitalized for severe acute respiratory syndrome coronavirus 2 infection, we analysed plasma markers of nervous system injury and astrocytic activation, measured 6 months post-infection: neurofilament light, glial fibrillary acidic protein and total tau protein. We assessed whether these markers were associated with the severity of the acute COVID-19 illness and with post-acute neuropsychiatric symptoms (as measured by the Patient Health Questionnaire for depression, the General Anxiety Disorder assessment for anxiety, the Montreal Cognitive Assessment for objective cognitive deficit and the cognitive items of the Patient Symptom Questionnaire for subjective cognitive deficit) at 6 months and 1 year post-hospital discharge from COVID-19. No robust associations were found between markers of nervous system injury and severity of acute COVID-19 (except for an association of small effect size between duration of admission and neurofilament light) nor with post-acute neuropsychiatric symptoms. These results suggest that ongoing neuropsychiatric symptoms are not due to ongoing neural injury