The epidemiology of injuries in Australian professional Rugby Union 2014 Super Rugby competition

BACKGROUND: Rugby union is a collision-based ball sport played at the professional level internationally. Rugby union has one of the highest reported incidences of injury of all team sports. PURPOSE: To identify the characteristics, incidence, and severity of injuries occurring in Australian professional Super Rugby Union. DESIGN: Descriptive epidemiology study. METHODS: The present study was a prospective epidemiology study on a cohort of 180 professional players from 5 Australian Super Rugby teams during the 2014 Super Rugby Union Tournament. Team medical staff collected and submitted daily training and match-play injury data through a secure, web-based electronic platform. The injury data included the main anatomic location of the injury, specific anatomic structure of the injury, injury diagnosis, training or match injury occurrence, main player position, mechanism of injury, and the severity of the injury quantified based on the number of days lost from training and/or competition due to injury. RESULTS: The total combined incidence rate for injury during training and match-play across all Australian Super Rugby Union teams was 6.96 per 1000 hours, with a mean injury severity of 37.45 days lost from training and competition. The match-play injury incidence rate was 66.07 per 1000 hours, with a mean severity of 39.80 days lost from training and competition. No significant differences were observed between forward- and back-playing positions for match or training injury incidence rate or severity. CONCLUSION: The incidence of injury for the present study was lower during match-play than has previously been reported in professional rugby union; however, the overall time loss was higher compared with previous studies in professional rugby union. The high overall time loss was due fundamentally to a high incidence of injuries with greater than 28 days’ severity

CNS Remyelination and the Innate Immune System.

A misguided inflammatory response is frequently implicated in myelin damage. Particularly prominent among myelin diseases, multiple sclerosis (MS) is an autoimmune condition, with immune-mediated damage central to its etiology. Nevertheless, a robust inflammatory response is also essential for the efficient regeneration of myelin sheaths after such injury. Here, we discuss the functions of inflammation that promote remyelination, and how these have been experimentally disentangled from the pathological facets of the immune response. We focus on the contributions that resident microglia and monocyte-derived macrophages make to remyelination and compare the roles of these two populations of innate immune cells. Finally, the current literature is framed in the context of developing therapies that manipulate the innate immune response to promote remyelination in clinical myelin disease.The authors would particularly like to acknowledge the support of the UK MS Society, The Jean Shanks Foundation and MedImmune.This is the author accepted manuscript. The final version is available from Frontiers via http://dx.doi.org/10.3389/fcell.2016.0003

Retinoid X receptor activation reverses age-related deficiencies in myelin debris phagocytosis and remyelination.

The efficiency of central nervous system remyelination declines with age. This is in part due to an age-associated decline in the phagocytic removal of myelin debris, which contains inhibitors of oligodendrocyte progenitor cell differentiation. In this study, we show that expression of genes involved in the retinoid X receptor pathway are decreased with ageing in both myelin-phagocytosing human monocytes and mouse macrophages using a combination of in vivo and in vitro approaches. Disruption of retinoid X receptor function in young macrophages, using the antagonist HX531, mimics ageing by reducing myelin debris uptake. Macrophage-specific RXRα (Rxra) knockout mice revealed that loss of function in young mice caused delayed myelin debris uptake and slowed remyelination after experimentally-induced demyelination. Alternatively, retinoid X receptor agonists partially restored myelin debris phagocytosis in aged macrophages. The agonist bexarotene, when used in concentrations achievable in human subjects, caused a reversion of the gene expression profile in multiple sclerosis patient monocytes to a more youthful profile and enhanced myelin debris phagocytosis by patient cells. These results reveal the retinoid X receptor pathway as a positive regulator of myelin debris clearance and a key player in the age-related decline in remyelination that may be targeted by available or newly-developed therapeutics.This work was supported by grants from the UK Multiple Sclerosis Society, Wellcome-Trust, NINDS/NIH Intramural Research Program, Health Research Board Scholars Program, Gates-Cambridge Scholarship, and Spanish Ministry of Economy and Competitiveness (SAF2012- 31483).S

Research Notes

http://deepblue.lib.umich.edu/bitstream/2027.42/61285/1/S_and_D-Spring_2007.pd

Change in CD3 positive T-cell expression in psoriatic arthritis synovium correlates with change in DAS28 and magnetic resonance imaging synovitis scores following initiation of biologic therapy - a single centre, open-label study

With the development of increasing numbers of potential therapeutic agents in inflammatory disease comes the need for effective biomarkers to help screen for drug efficacy and optimal dosing regimens early in the clinical trial process. This need has been recognized by the Outcome Measures in Rheumatology Clinical Trials (OMERACT) group, which has established guidelines for biomarker validation. To seek a candidate synovial biomarker of treatment response in psoriatic arthritis (PsA), we determined whether changes in immunohistochemical markers of synovial inflammation correlate with changes in disease activity scores assessing 28 joints (ΔDAS28) or magnetic resonance imaging synovitis scores (ΔMRI) in patients with PsA treated with a biologic agent. Twenty-five consecutive patients with PsA underwent arthroscopic synovial biopsies and MRI scans of an inflamed knee joint at baseline and 12 weeks after starting treatment with either anakinra (first 10 patients) or etanercept (subsequent 15 patients) in two sequential studies of identical design. DAS28 scores were measured at both time points. Immunohistochemical staining for CD3, CD68 and Factor VIII (FVIII) was performed on synovial samples and scored by digital image analysis (DIA). MRI scans performed at baseline and at 12 weeks were scored for synovitis semi-quantitatively. The ΔDAS28 of the European League Against Rheumatism good response definition (>1.2) was chosen to divide patients into responder and non-responder groups. Differences between groups (Mann Whitney U test) and correlations between ΔDAS28 with change in immunohistochemical and MRI synovitis scores (Spearman's rho test) were calculated. Paired synovial samples and MRI scans were available for 21 patients (8 anakinra, 13 etanercept) and 23 patients (8 anakinra, 15 etanercept) respectively. Change in CD3 (ΔCD3) and CD68 expression in the synovial sublining layer (ΔCD68sl) was significantly greater in the disease responders compared to non-responders following treatment (P = 0.005 and 0.013 respectively). ΔCD3, but not ΔCD68 or ΔFVIII, correlated with both ΔDAS28 (r = 0.49, P = 0.025) and ΔMRI (r = 0.58, P = 0.009). The correlation of ΔCD3 with ΔDAS28 and ΔMRI following biologic treatment in this cohort contributes to the validation of ΔCD3 as a synovial biomarker of disease response in PsA, and supports the further evaluation of ΔCD3 for predictive properties of future clinical outcome

Changes in the Oligodendrocyte Progenitor Cell Proteome with Ageing.

Following central nervous system (CNS) demyelination, adult oligodendrocyte progenitor cells (OPCs) can differentiate into new myelin-forming oligodendrocytes in a regenerative process called remyelination. Although remyelination is very efficient in young adults, its efficiency declines progressively with ageing. Here we performed proteomic analysis of OPCs freshly isolated from the brains of neonate, young and aged female rats. Approximately 50% of the proteins are expressed at different levels in OPCs from neonates compared with their adult counterparts. The amount of myelin-associated proteins, and proteins associated with oxidative phosphorylation, inflammatory responses and actin cytoskeletal organization increased with age, whereas cholesterol-biosynthesis, transcription factors and cell cycle proteins decreased. Our experiments provide the first ageing OPC proteome, revealing the distinct features of OPCs at different ages. These studies provide new insights into why remyelination efficiency declines with ageing and potential roles for aged OPCs in other neurodegenerative diseases

Reprogramming within Hours Following Nuclear Transfer into Mouse but not Human Zygotes

Fertilized mouse zygotes can reprogram somatic cells to a pluripotent state. Human zygotes might therefore be useful for producing patient-derived pluripotent stem cells. However, logistical, legal and social considerations have limited the availability of human eggs for research. Here we show that a significant number of normal fertilized eggs (zygotes) can be obtained for reprogramming studies. Using these zygotes, we found that when the zygotic genome was replaced with that of a somatic cell, development progressed normally throughout the cleavage stages, but then arrested before the morula stage. This arrest was associated with a failure to activate transcription in the transferred somatic genome. In contrast to human zygotes, mouse zygotes reprogrammed the somatic cell genome to a pluripotent state within hours after transfer. Our results suggest that there may be a previously unappreciated barrier to successful human nuclear transfer, and that future studies could focus on the requirements for genome activation.Stem Cell and Regenerative Biolog

Gene Banks, Seed Libraries, and Vegetable Sanctuaries: The Cultivation and Conservation of Heritage Vegetables in Britain, 1970–1985

Individual seed saving and exchange are considered important components of contemporary efforts to conserve crop genetic diversity, which ramify at local, regional, and global scales. Yet the very fact that the contributions of these activities to conservation need to be made explicit by seed savers and those who study them indicates that the practices of seed saving and exchange may not immediately be recognized as conservation-oriented activities. This article investigates why and how individual seed saving came to be aligned with a broader conservation agenda in Britain through an historical examination of the promotion of seed saving by the Henry Doubleday Research Association (HDRA) in the 1970s and 1980s. It demonstrates how several HDRA initiatives that aimed to preserve vegetable diversity also re-inscribed British gardeners' ordinary labor as conservation work. This historical study complements sociological and ethnographic studies, highlighting the role of a prominent organization in creating pathways for individuals to engage in local, national, and international conservation through seed saving. It also serves as a reminder that the connections between these activities had to be made explicit—that is, that there was (and is) work involved in connecting individual acts of seed saving to conservation outcomes at different scales