518 research outputs found

    b-Quark Production in Proton-Proton Collisions at Center of Mass Energies of 510 GeV in the PHENIX Detector at RHIC

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    Heavy flavor quarks are an important probe of the initial state of the Quark Gluon Plasma formed in heavy-ion collisions. Bottom and charm quarks are produced early in the collision, primarily through hard interactions, and experience the full time evolution of the medium. Understanding bottom quark production in proton-proton collisions gives a baseline reference for studying larger collision systems. The measurement of the b-quark production ∆φ correlations gives insight into the b-quark production mechanisms. The signal can be isolated by taking advantage of the properties of neutral B meson oscillations in the invariant mass region of 5-10 GeV. Measuring like-sign dimuons within this mass range provides an enriched bottom signal with a minimal amount of open charm background and without any contributions from quarkonia or Drell-Yan pairs. b-quark production will be measured through the semi-leptonic decay like-sign dimuon signal, in the rapidity range 1.2 \u3c |y| \u3c 2.2 and at √s = 510 GeV from data recorded in 2013 at the PHENIX experiment. The measured total cross section is 14.9 ± 0.7(stat) ± 2.0(type B sys.) ± 3.4(type C sys.)[μb]

    Scintillator-Based UAV

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    Marsupialisation of 12 odontogenic cysts in Boxer dogs: Retrospective case series

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    Marsupialisation of odontogenic cysts is a minimally invasive treatment method used in human dentistry. Marsupialisation decompresses the cyst and promotes remodeling of alveolar bone and shrinkage of the cyst. In this retrospective study we look at the effectiveness of marsupialisation at reducing the size of odontogenic cysts in dogs. The case series consists of six Boxer dogs with 12 odontogenic cysts. Each case underwent a high resolution CT scan prior to treatment and at follow-up. Each CT scan was reviewed, the volume of each cyst calculated using manual segmentation and the reduction in cyst volume calculated. There was a marked reduction in cystic volume of 66.6% over a mean of 138 days. This shows that the use of marsupialisation effective method of reducing cyst volume

    Dietary nitrate reduces muscle metabolic perturbation and improves exercise tolerance in hypoxia

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    The definitive version is available at www3.interscience.wiley.comExercise in hypoxia is associated with reduced muscle oxidative function and impaired exercise tolerance. We hypothesised that dietary nitrate supplementation (which increases plasma [nitrite] and thus NO bioavailability) would ameliorate the adverse effects of hypoxia on muscle metabolism and oxidative function. In a double-blind, randomised crossover study, nine healthy subjects completed knee-extension exercise to the limit of tolerance (T(lim)), once in normoxia (20.9% O(2); CON) and twice in hypoxia (14.5% O(2)). During 24 h prior to the hypoxia trials, subjects consumed 0.75 L of nitrate-rich beetroot juice (9.3 mmol nitrate; H-BR) or 0.75 L of nitrate-depleted beetroot juice as a placebo (0.006 mmol nitrate; H-PL). Muscle metabolism was assessed using calibrated (31)P-MRS. Plasma [nitrite] was elevated (P < 0.01) following BR (194 ± 51 nm) compared to PL (129 ± 23 nm) and CON (142 ± 37 nM). T(lim) was reduced in H-PL compared to CON (393 ± 169 vs. 471 ± 200 s; P < 0.05) but was not different between CON and H-BR (477 ± 200 s). The muscle [PCr], [P(i)] and pH changed at a faster rate in H-PL compared to CON and H-BR. The [PCr] recovery time constant was greater (P < 0.01) in H-PL (29 ± 5 s) compared to CON (23 ± 5 s) and H-BR (24 ± 5 s). Nitrate supplementation reduced muscle metabolic perturbation during exercise in hypoxia and restored exercise tolerance and oxidative function to values observed in normoxia. The results suggest that augmenting the nitrate-nitrite-NO pathway may have important therapeutic applications for improving muscle energetics and functional capacity in hypoxia

    Intrasynovial triamcinolone treatment is not associated with incidence of acute laminitis

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    Background: Intra-synovial corticosteroid injections are commonly used in the treatment of equine orthopaedic disease, but corticosteroid administration is widely considered a risk factor for the development of laminitis. Despite a list of putative mechanisms and a number of case reports of steroid-induced laminitis, no case-control or cohort studies investigating the association between use of intra-synovial corticosteroids and acute laminitis have been published. Objectives: To quantify the risk of laminitis posed by intra-synovial triamcinolone acetonide (TA) administration in a mixed population of horses. Study design: Retrospective observational cohort study. Methods: Clinical records of horses registered with one large UK equine practice were reviewed retrospectively to identify all horses receiving intra-synovial TA treatment between 1 January 2007 and 31 December 2017. 1,510 horses were selected and records investigated for incidence of laminitis over a 4-month period following treatment. For each TA-treated horse, an untreated horse, individually matched by age, sex, date of treatment and client type, was selected from the clinical records. Untreated horses were then investigated for laminitis over the same 4-month period. Data was analysed in a 2×2 contingency table using Fisher’s exact test. Results: 489 horses were lost to follow-up and 55 horses were excluded, leaving 966 treated and matched, untreated horses. The incidence of laminitis over the 4-month study period in both groups was identical: 3/966 horses (0.31%) (95% C.I. [0.08%, 0.91%]), equivalent to 0.93 cases per 100 horses per year (P >0.9). Main limitations: Retrospective study; large proportion (489/1510) of horses lost to follow-up; large proportion of study population were racehorses; selection method resulted in disproportionate selection of horses born before 2013; similar incidence between groups may reflect existing risk-based selection by clinicians. Conclusions: Intra-synovial triamcinolone acetonide administration does not increase the risk of laminitis in this study population

    Evidence in support of the call to ban the tackle and harmful contact in school rugby: a response to World Rugby

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    In a paper published in BJSM (June 2016), World Rugby employees Ross Tucker and Martin Raftery and a third coauthor Evert Verhagen took issue with the recent call to ban tackling in school rugby in the UK and Ireland. That call (to ban tackling) was supported by a systematic review published in BJSM. Tucker et al claim that: (1) the mechanisms and risk factors for injury along with the incidence and severity of injury in youth rugby union have not been thoroughly identified or understood; (2) rugby players are at no greater risk of injury than other sports people, (3) this is particularly the case for children under 15 years and (4) removing the opportunity to learn the tackle from school pupils might increase rates of injuries. They conclude that a ban ‘may be unnecessary and may also lead to unintended consequences such as an increase in the risk of injury later in participation.’ Here we aim to rebut the case by Tucker et al. We share new research that extends the findings of our original systematic review and meta-analysis. A cautionary approach requires the removal of the tackle from school rugby as the quickest and most effective method of reducing high injury rates in youth rugby, a public health priority

    Tackle-related injury rates and nature of injuries in South African Youth Week tournament rugby union players (under-13 to under-18): an observational cohort study.

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    OBJECTIVES: The tackle situation is most often associated with the high injury rates in rugby union. Tackle injury epidemiology in rugby union has previously been focused on senior cohorts but less is known about younger cohorts. The aim of this study was to report on the nature and rates of tackle-related injuries in South African youth rugby union players representing their provinces at national tournaments. DESIGN: Observational cohort study. SETTING: Four South African Youth Week tournaments (under-13 Craven Week, under-16 Grant Khomo Week, under-18 Academy Week, under-18 Craven Week). PARTICIPANTS: Injury data were collected from 3652 youth rugby union players (population at risk) in 2011 and 2012. OUTCOME MEASURES: Tackle-related injury severity ('time-loss' and 'medical attention'), type and location, injury rate per 1000 h (including 95% CIs). Injury rate ratios (IRR) were calculated and modelled using a Poisson regression. A χ(2) analysis was used to detect linear trends between injuries and increasing match quarters. RESULTS: The 2012 under-13 Craven Week had a significantly greater 'time-loss' injury rate when compared with the 2012 under-18 Academy Week (IRR=4.43; 95% CI 2.13 to 9.21, p<0.05) and under-18 Craven Week (IRR=3.52; 95% CI 1.54 to 8.00, p<0.05). The Poisson regression also revealed a higher probability of 'overall' ('time-loss' and 'medical attention' combined) and 'time-loss' tackle-related injuries occurring at the under-13 Craven Week. The proportion of 'overall' and 'time-loss' injuries increased significantly with each quarter of the match when all four tournaments were combined (p<0.05). CONCLUSIONS: There was a difference in the tackle-related injury rate between the under-13 tournament and the two under-18 tournaments, and the tackle-related injury rate was higher in the final quarter of matches. Ongoing injury surveillance is required to better interpret these findings. Injury prevention strategies targeting the tackle may only be effective once the rate and nature of injuries have been accurately determined

    Severity of arterial hypoxaemia affects the relative contributions of peripheral muscle fatigue to exercise performance in healthy humans

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    This article has been made available through the Brunel Open Access Publishing Fund and is available from the specified link - Copyright @ 2007 The Physiological Society.We examined the effects of hypoxia severity on peripheral versus central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various fractions of inspired O-2 fraction (F-IO2 0.21/0.15/0.10). At task failure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O-2 supplementation (F-IO2 = 0.30) and subjects were encouraged to continue exercising. Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (Delta Q(tw,pot)) as measured pre- versus post-exercise in response to supramaximal femoralnerve stimulation. At task failure in normoxia (haemoglobin saturation (S-pO2) similar to 94%, 656 +/- 82 s) and moderate hypoxia (S-pO2 similar to 82%, 278 +/- 16 s), hyperoxygenation had no significant effect on prolonging endurance time. However, following task failure in severe hypoxia (S-pO2, similar to 67%; 125 +/- 6 s), hyperoxygenation elicited a significant prolongation of time to exhaustion (171 6 1 %). The magnitude of A Q(tw,pot) at exhaustion was not different among the three trials (-35% to -36%, P = 0.8). Furthermore, quadriceps integrated EMG, blood lactate, heart rate, and effort perceptions all rose significantly throughout exercise, and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe hypoxia, we repeated this trial and assessed peripheral fatigue following task failure prior to hyperoxygenation (125 +/- 6 s). Although Q(tw,pot) was reduced from pre-exercise baseline (-23%; P < 0.01), peripheral fatigue was substantially less (P < 0.01) than that observed at task failure in normoxia and moderate hypoxia. We conclude that across the range of normoxia to severe hypoxia, the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxia-sensitive central component of fatigue, probably involving brain hypoxic effects on effort perception.This research was supported by a National Heart, Lung, and Blood Institute (NHLBI) RO1 grant (HL-15469)
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