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Objective To investigate the differences between skeletal and chronological age and to assess the role of maturity status, anthropometric data, and football related variables in explaining injury statistics in elite schoolboy footballers.Design Prospective study of injuries in schoolboy footballers according to skeletal age.Setting Premier league football club in England.Participants 292 schoolboy players (age 9-16) registered at the clubInterventions Annual x ray film of hand or wrist.Main outcome measures Data on injury 2001-7. Skeletal age determined with the Fels method. Skeletal age of more than one year above chronological age was classified as an early maturer, within one year as a normal maturer, and more than one year below normal as a late maturer. Injury and hours of training and rates of exposure to match play.Results Over six years 476 injuries were reported. The mean chronological age (11.74 (SD 2.35) years) and skeletal age defined by x ray picture (12.08 (SD 3.14) years) showed a significant mean difference of −0.344 (95% confidence interval −0.490 to −0.198; t=−4.64, df=280). Analysis of covariance showed that injury incidents did not differ significantly with maturity status after adjusting for training time, playing time, height, and position played (F=0.32,160, P=0.73). General log linear analysis with a Poisson model showed that difference in maturity, playing hours, and training hours collectively explained 48% of the variance in injury incidents. Injury exposure rates differed considerably, with 1.44/1000 hours for training and 10.5/1000 hours for match play.Conclusion Maturity, defined by the difference between chronological age and skeletal age, plus training and playing hours together predict injury in schoolboy footballers. Injury exposure rates were higher for match play than training, which could have implications for targeting preventative interventions by academy staff. The use of skeletal age measurements to establish accurate “windows of opportunity” for training is more appropriate than the commonly used chronological age. Caution is needed when interpreting differences in injury occurrence as the factors that contribute are often complex.

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Peroxisome proliferator–activated receptors (PPARs; PPAR-α, PPAR-δ, and PPAR-γ) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-δ, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR-δ (PPAR-δ−/−) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-γ+IL-17A− and IFN-γ+IL-17A+ CD4+ cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-δ−/− mice occurred as a result of a constellation of immune system aberrations that included higher CD4+ cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR-δ in inhibiting the production of IFN-γ and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR-δ serves as an important molecular brake for the control of autoimmune inflammation.

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, over 7 million confirmed cases and over 400,000 deaths had been recorded across 213 countries and territories [3]. In outbreaks, epidemics, and pandemics, epidemiologists aim to quantify the spread of a disease within a population across space and time. In addition, epidemiologists aim to quantify the rate of disease transmission. This information is then used to inform prevention and mitigation strategies. Although aggressive prevention strategies may be disruptive and costly, such measures may ultimately reduce the burden of morbidity and mortality within a population, as has been demonstrated in previous pandemics, such as the 1918-1920 influenza and the 2009 influenza A (H1N1) pandemics [4, 5]. The first tier of response is containment to prevent the spread of disease before it has a chance to take hold in the community [6]. This may include contact tracing, surveillance in the community through widespread testing, and quarantine measures. However, once a disease has spread through the community, the second tier, mitigation strategies, are necessary to reduce transmission. Interventions include social distancing measures; closure of schools, workplaces, and community facilities; travel restrictions; and individual-level hygiene measures, such as wearing a mask and washing hands [6]. Without mitigation efforts in place, healthcare systems risk being stretched beyond capacity in, for example, intensive care unit (ICU) beds, personal protective equipment (PPE), and ventilators for treating patients with COVID-19. This is why countries who were in the mitigation phase of the pandemic conducted communication campaigns imploring individuals to engage in behaviors to "flatten the curve." Beyond the mitigation tier, state-level actors may put lockdowns in place to further curb transmission. Scope of the problem Asia Countries across Asia were some of the first to experience the outbreak of COVID-19. Many had already had previous experiences dealing with epidemics, including severe acute respiratory syndrome (SARS) from 2002 to 2003, H1N1 flu in 2009, and Middle East Respiratory Syndrome (MERS) in 2014, 2015 and 2018 [7]. Such experiences had prepared governments to respond and made their populations more receptive to restrictive public health measures. Some entities, including South Korea, Mongolia, Hong Kong, and Singapore, initially succeeded in containing the virus through aggressive preemptive measures: transparency in communication, ubiquitous testing, strict quarantine, and thorough disinfectant protocols [7, 8]. South Korea used such measures without ever putting a lockdown in place. After failures in communication during the MERS epidemic in 2015, new standard operating procedures were put in place. By the time COVID-19 arrived, Koreans were willing to

Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain, and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids’ saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS.

BackgroundThe pathogenesis of the Osgood-Schlatter's disease (OSD) is still debated. The fragmentation of the ossification centre has been questioned as a definitive sign of OSD and has been seen as a normal development of the anterior tibial tubercle (ATT).ObjectivesIt is unknown if such changes are present in the presumed pathological tendon insertion seen in OSD, nor the relation of Doppler-positive changes to pain on clinical examination.MethodsA prospective analysis was carried out on 20 consecutive symptomatic male athletes (13.9 years±1.3) and a comparison group of asymptomatic subjects. All underwent a comparative clinical assessment and ultrasound with colour Doppler scan on both knees. Subjective pain was recorded with a visual analogue scale (VAS) during provocative manoeuvres: palpation, resisted contraction and single leg squat.ResultsPositive Doppler US (within the distal end of the patellar tendon) was associated with higher pain on palpation (47±24.5 vs 18±11.4, p<0.01) and resisted static contraction (59±20.2 vs 27±12.5, p<0.001) compared with Doppler-negative subjects. No Doppler activity was found in the comparison group. VAS for palpation and resisted contraction of the athletes graded as stage 2 (51.1±22.0 and 60.0±21.2) were significantly higher than stage 3 (17.8±12.0 and 18.9±16.9) and stage 4 (15.0±7.1 and 25.0±7.1; p<0.01).ConclusionsMore painful OSD is associated with the presence of neo-vessels. This may be linked with a particular stage of ATT maturation and applied compressive forces. A Doppler ultrasound scan adds practical information to develop the care plan of the patient.