140 research outputs found
Youth, community and social well-being: Investigating the role of youth groups in the health and social well-being of young in semi-rural areas in the North of England
Characterisation of football trajectories for assessing flight performance
Much discussion surrounds the flight of association footballs (soccer balls), particularly where the flight may be perceived as irregular. This is particularly prevalent in high profile competitions due to increased camera coverage and public scrutiny. Footballs do not all perform in an identical manner in-flight. This paper develops methods to characterise the important features of flight, enabling direct, quantitative comparisons between ball designs. The system used to generate the flight paths included collection of aerodynamic force coefficient data in a wind tunnel, which were input into a flight model across a wide range of realistic conditions. Parameters were derived from these trajectories to characterise the in-flight deviations across the range of flights from which the aerodynamic performance of different balls were statistically compared. The amount of lateral movement in-flight was determined by calculating the final lateral deviation from the initial shot vector. To quantify the overall shape of the flight, increasing orders of polynomial functions were fitted to the flight path until a good fit was obtained with a high order polynomial indicating a less consistent flight. The number of inflection points in each flight was also recorded to further define the flight path. The orientation dependency of a ball was assessed by comparing the true shot to a second flight path without considering orientation dependent forces. The difference between these flights isolated the effect of orientation dependent aerodynamic forces. The paper provides the means of quantitatively describing a ball’s aerodynamic behaviour in a defined and robust mathematical process. Conclusions were not drawn regarding which balls are good and bad; these are subjective terms and can only be analysed through comprehensive player perception studies
Cerebral haemodynamics during experimental intracranial hypertension.
Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline (∼9 mmHg; SE 1.5) to moderate intracranial pressure (∼41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45 cm/s; p = 0.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p < 0.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p < 0.001; wall tension 19.3 to 9.8 mmHg, p < 0.001). From moderate to high intracranial pressure (∼75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3 cm/s p < 0.001, laser Doppler flowmetry 39.1 to 13.3%, p < 0.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p < 0.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p = 0.35).This animal model of acute intracranial hypertension demonstrated two intracranial pressure-dependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.The authors would acknowledge Dr Hugh Richards and Dr Stefan Piechnik who contributed to data collection. JD is supported by a Woolf Fisher scholarship. GVV is supported by an A.G. Leventis Foundation Scholarship, and a Charter Studentship from St Edmund’s College, Cambridge. XYL is supported by Bill Gates Scholarship, and DC is supported by a Cambridge Commonwealth, European & International Trust Scholarship (University of Cambridge).This is the author accepted manuscript. The final version is available from SAGE via https://doi.org/10.1177/0271678X1663906
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Increased ICP and Its Cerebral Haemodynamic Sequelae.
OBJECTIVES: Increased intracranial pressure (ICP) is a pathological feature of many neurological diseases; however, the local and systemic sequelae of raised ICP are incompletely understood. Using an experimental paradigm, we aimed to describe the cerebrovascular consequences of acute increases in ICP. MATERIALS AND METHODS: We assessed cerebral haemodynamics [mean arterial blood pressure (MAP), ICP, laser Doppler flowmetry (LDF), basilar artery Doppler flow velocity (Fv) and estimated vascular wall tension (WT)] in 27 basilar artery-dependent rabbits during experimental (artificial lumbar CSF infusion) intracranial hypertension. WT was estimated as the difference between critical closing pressure and ICP. RESULTS: From baseline (~9 mmHg) to moderate increases in ICP (~41 mmHg), cortical LDF decreased (from 100 to 39.1%, p < 0.001), while mean global Fv was unchanged (from 47 to 45 cm/s, p = 0.38). In addition, MAP increased (from 88.8 to 94.2 mmHg, p < 0.01 and WT decreased (from 19.3 to 9.8 mmHg, p < 0.001). From moderate to high ICP (~75 mmHg), both global Fv and cortical LDF decreased (Fv, from 45 to 31.3 cm/s, p < 0.001; LDF, from 39.1 to 13.3%, p < 0.001) while MAP increased further (94.2 to 114.5 mmHg, p < 0.001) and estimated WT was unchanged (from 9.7 to 9.6 mmHg, p = 0.35). CONCLUSION: In this analysis, we demonstrate a cortical vulnerability to increases in ICP and two ICP-dependent cerebro-protective mechanisms: with moderate increases in ICP, WT decreases and MAP increases to buffer cerebral perfusion, while with severe increases of ICP, an increased MAP predominates
Palaeomagnetism and magnetostiatigraphy of Triassic strata in the Sangre de Cristo Mountains and Tucumcari Basin, New Mexico, USA
We report palaeomagnetic data and a composite magnetic polarity sequence for Middle and Upper Triassic rocks assigned to the Anton Chico Member of the Moenkopi Formation and Chinle Group, respectively, exposed along the eastern flank of the Sangre de Cristo Mountains and in the Tucumcari Basin of eastern and northeastern New Mexico. Thermal demagnetization isolates a well-defined, dual polarity, characteristic magnetization, carried in most cases by haematite and interpreted as an early acquired chemical remanent magnetization (CRM). Characteristic magnetizations from 74 palaeomagnetic sites (one site = one bed) are used to define a magnetic polarity sequence, which we correlate with previously published Triassic data obtained from both marine and non-marine rocks. Preliminary correlation suggests that the resolution of magnetostratigraphic data derived from continental strata is not necessarily of lesser quality than that from marine rocks. On the basis of the magnetostratigraphic data, a profound unconformity is believed to separate lower-middle Norian and upper Norian-Rhaetian strata of the Chinle Group. Palaeomagnetic poles derived from selected sites in steeply dipping (> 85°) strata for the Middle Triassic (Anisian, ∼240 Ma: 50°N 121°E; N = 8), late Carman-early Norian (∼225 Ma: 53°N 104°E; N = 16), and late Norian-Rhaetian (∼208 Ma: 59°N 77°E; N = 8) are in relatively good agreement with previously published data for the Moenkopi Formation and Chinle Group and related strata in southwest North America. None the less, comparison with palaeomagnetic poles obtained from gently dipping or flat-lying Triassic strata from this study (Anisian, 46°N 112°E; N = 13; late Carnian, 54°N 87°E; N =12) and previously published Triassic poles in southwest North America suggest that a modest ‘apparent rotation’ not greater than about 5° affects declinations from steeply dipping rocks. The distribution of palaeomagnetic poles indicates ∼25° (angular distance) of apparent polar wander between about 240 and 208 Ma.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73972/1/j.1365-246X.1996.tb05646.x.pd
New constraints on equatorial temperatures during a Late Neoproterozoic snowball Earth glaciation
Search for black holes and other new phenomena in high-multiplicity final states in proton-proton collisions at root s=13 TeV
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Effect of Hydrocortisone on Mortality and Organ Support in Patients With Severe COVID-19: The REMAP-CAP COVID-19 Corticosteroid Domain Randomized Clinical Trial.
Importance: Evidence regarding corticosteroid use for severe coronavirus disease 2019 (COVID-19) is limited. Objective: To determine whether hydrocortisone improves outcome for patients with severe COVID-19. Design, Setting, and Participants: An ongoing adaptive platform trial testing multiple interventions within multiple therapeutic domains, for example, antiviral agents, corticosteroids, or immunoglobulin. Between March 9 and June 17, 2020, 614 adult patients with suspected or confirmed COVID-19 were enrolled and randomized within at least 1 domain following admission to an intensive care unit (ICU) for respiratory or cardiovascular organ support at 121 sites in 8 countries. Of these, 403 were randomized to open-label interventions within the corticosteroid domain. The domain was halted after results from another trial were released. Follow-up ended August 12, 2020. Interventions: The corticosteroid domain randomized participants to a fixed 7-day course of intravenous hydrocortisone (50 mg or 100 mg every 6 hours) (n = 143), a shock-dependent course (50 mg every 6 hours when shock was clinically evident) (n = 152), or no hydrocortisone (n = 108). Main Outcomes and Measures: The primary end point was organ support-free days (days alive and free of ICU-based respiratory or cardiovascular support) within 21 days, where patients who died were assigned -1 day. The primary analysis was a bayesian cumulative logistic model that included all patients enrolled with severe COVID-19, adjusting for age, sex, site, region, time, assignment to interventions within other domains, and domain and intervention eligibility. Superiority was defined as the posterior probability of an odds ratio greater than 1 (threshold for trial conclusion of superiority >99%). Results: After excluding 19 participants who withdrew consent, there were 384 patients (mean age, 60 years; 29% female) randomized to the fixed-dose (n = 137), shock-dependent (n = 146), and no (n = 101) hydrocortisone groups; 379 (99%) completed the study and were included in the analysis. The mean age for the 3 groups ranged between 59.5 and 60.4 years; most patients were male (range, 70.6%-71.5%); mean body mass index ranged between 29.7 and 30.9; and patients receiving mechanical ventilation ranged between 50.0% and 63.5%. For the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively, the median organ support-free days were 0 (IQR, -1 to 15), 0 (IQR, -1 to 13), and 0 (-1 to 11) days (composed of 30%, 26%, and 33% mortality rates and 11.5, 9.5, and 6 median organ support-free days among survivors). The median adjusted odds ratio and bayesian probability of superiority were 1.43 (95% credible interval, 0.91-2.27) and 93% for fixed-dose hydrocortisone, respectively, and were 1.22 (95% credible interval, 0.76-1.94) and 80% for shock-dependent hydrocortisone compared with no hydrocortisone. Serious adverse events were reported in 4 (3%), 5 (3%), and 1 (1%) patients in the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively. Conclusions and Relevance: Among patients with severe COVID-19, treatment with a 7-day fixed-dose course of hydrocortisone or shock-dependent dosing of hydrocortisone, compared with no hydrocortisone, resulted in 93% and 80% probabilities of superiority with regard to the odds of improvement in organ support-free days within 21 days. However, the trial was stopped early and no treatment strategy met prespecified criteria for statistical superiority, precluding definitive conclusions. Trial Registration: ClinicalTrials.gov Identifier: NCT02735707
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