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    <title>STORRE Collection: Electronic copies of Faculty of Health Sciences and Sport book chapters and sections.</title>
    <link>http://hdl.handle.net/1893/621</link>
    <description>Electronic copies of Faculty of Health Sciences and Sport book chapters and sections.</description>
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        <rdf:li rdf:resource="http://hdl.handle.net/1893/37815" />
        <rdf:li rdf:resource="http://hdl.handle.net/1893/37697" />
        <rdf:li rdf:resource="http://hdl.handle.net/1893/37696" />
        <rdf:li rdf:resource="http://hdl.handle.net/1893/37689" />
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    <dc:date>2026-09-26T01:55:43Z</dc:date>
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    <title>Parental Problem Drug Use</title>
    <link>http://hdl.handle.net/1893/37815</link>
    <description>Title: Parental Problem Drug Use
Author(s): Whittaker, Anne
Editor(s): Taylor, Julie; Themessi-Huber, Markus
Abstract: First paragraph:  Primary Care has an important role in the care of children and families affected by parental problem drug use. This chapter focuses on the skills required to work effectively with drug-using parents. It aims to complement guidance on working with children, and includes an overview of drug policy and drug treatment, the scale and nature of the problem, a framework for care and good practice, and examples of harm reduction strategies and interventions. The chapter draws on evidence from impact and intervention studies on parental problem drug use, as well as qualitative research on drug-using parents and their families. Findings from the author’s own qualitative research study involving drug-using fathers are incorporated.</description>
    <dc:date>2009-01-01T00:00:00Z</dc:date>
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  <item rdf:about="http://hdl.handle.net/1893/37697">
    <title>The genetic association with exercise-induced muscle damage and muscle injury risk</title>
    <link>http://hdl.handle.net/1893/37697</link>
    <description>Title: The genetic association with exercise-induced muscle damage and muscle injury risk
Author(s): Baumert, Philipp; Hall, Elliott C R; Erskine, Robert M
Abstract: An athlete's potential to succeed at the highest level of sport may be determined in part by their physical resilience, such as their ability to recover quickly from training/competition, and their robustness regarding injury risk, particularly concerning muscle tissue. There is evidence to suggest that a high individual variability exists in (i) the response to exercise-induced muscle damage (EIMD) and (ii) muscle injury risk; and differences in genetic make-up might explain some of this variation. This chapter summarizes the current evidence regarding associations between genetic variation and the individual response following EIMD, and the risk of suffering muscle injuries. Further, this chapter proposes a new potential mechanical mechanism underlying skeletal muscle's maladaptation to strenuous exercise, thus providing a better understanding of the tissue-specific contribution to EIMD, exertional rhabdomyolysis and muscle strain injury.</description>
    <dc:date>2020-01-01T00:00:00Z</dc:date>
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  <item rdf:about="http://hdl.handle.net/1893/37696">
    <title>Advances in Sports Genomics</title>
    <link>http://hdl.handle.net/1893/37696</link>
    <description>Title: Advances in Sports Genomics
Author(s): Ahmetov, Ildus I; Hall, Elliott C R; Semenova, Ekaterina A; Pranckevičienė, Erinija; Ginevičienė, Valentina
Abstract: Sports genomics is the scientific discipline that focuses on the organization and function of the genome in elite athletes, and aims to develop molecular methods for talent identification, personalized exercise training, nutritional need and prevention of exercise-related diseases. It postulates that both genetic and environmental factors play a key role in athletic performance and related phenotypes. This update on the panel of genetic markers (DNA polymorphisms) associated with athlete status and soft-tissue injuries covers advances in research reported in recent years, including one whole genome sequencing (WGS) and four genome-wide association (GWAS) studies, as well as findings from collaborative projects and meta-analyses. At end of 2020, the total number of DNA polymorphisms associated with athlete status was 220, of which 97 markers have been found significant in at least two studies (35 endurance-related, 24 power-related, and 38 strength-related). Furthermore, 29 genetic markers have been linked to soft-tissue injuries in at least two studies. The most promising genetic markers include HFE rs1799945, MYBPC3 rs1052373, NFIA-AS2 rs1572312, PPARA rs4253778, and PPARGC1A rs8192678 for endurance; ACTN3 rs1815739, AMPD1 rs17602729, CPNE5 rs3213537, CKM rs8111989, and NOS3 rs2070744 for power; LRPPRC rs10186876, MMS22L rs9320823, PHACTR1 rs6905419, and PPARG rs1801282 for strength; and COL1A1 rs1800012, COL5A1 rs12722, COL12A1 rs970547, MMP1 rs1799750, MMP3 rs679620, and TIMP2 rs4789932 for soft-tissue injuries. It should be appreciated, however, that hundreds and even thousands of DNA polymorphisms are needed for the prediction of athletic performance and injury risk.</description>
    <dc:date>2022-01-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://hdl.handle.net/1893/37689">
    <title>SALUTOGENESIS: The Foundation for Supporting the Young Athlete</title>
    <link>http://hdl.handle.net/1893/37689</link>
    <description>Title: SALUTOGENESIS: The Foundation for Supporting the Young Athlete
Author(s): Kirkland, Andrew
Editor(s): Borrie, Andy; Ryall, Emily
Abstract: First paragraph: In their International Olympic Committee Consensus Statement, Bergeron et al. (2015) suggest that the goal of sport is clear, to:  Develop healthy, capable and resilient young athletes, whilst attaining wide-spread, inclusive, sustainable participation and success for all levels of individual athletic achievement.  The premise of this book, however, is that talent development programmes usually fail to achieve this goal. Reasons for such failures relate not only to the fallibilities of humans but also to the complexity of human adaptation.</description>
    <dc:date>2025-01-01T00:00:00Z</dc:date>
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