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- Helland, C., et al.
(author)
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Force-velocity profiling of sprinting athletes: single-run vs. multiple-run methods
- 2019
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In: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 119:2, s. 465-473
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Journal article (peer-reviewed)abstract
- Purpose This study explored the agreement between a single-run and a multiple-run method for force-velocity (Fv) profiling of sprinting athletes; we evaluated both absolute values and changes over time caused by sprint training. Methods Seventeen female handball players (23 +/- 3 years, 177 +/- 7 cm, 73 +/- 6 kg) performed 30 m un-resisted and resisted sprints (50, 80 and 110 N resistance) before and after an 8-week sprint training intervention. Two approaches were used to calculate theoretical maximal velocity (v0), horizontal force (F0), power (Pmax), and the force-velocity slope (SFv): (1) the single-run method, based on inverse dynamics applied to the centre-of-mass movement, was calculated from anthropometric and sprint split time data; and (2) the multiple-run method, where peak velocity from un-resisted and resisted sprints were plotted against the horizontal resistances. Results Trivial differences in v0 (0.7%) were observed between the two calculation methods. Corresponding differences for F0, Pmax and SFv were 16.4, 15.6 and 17.6%, respectively (most likely; very large effect size). F0 showed poor agreement between the methods (r = 0.26 and 0.16 before and after the intervention). No substantial correlation between the changes (from pre-to post-training tests) in SFV calculated with the single-run and the multiple-run methods were observed (r = 0.02). Conclusions This study revealed poor agreement between the Fv relationships of the investigated calculation methods. In practice, both methods may have a purpose, but the single-run and the multiple-run methods appear to measure somewhat different sprint properties and cannot be used interchangeably.
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- Wanschers, Bas F. J., et al.
(author)
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A mutation in the human CBP4 ortholog UQCC3 impairs complex III assembly, activity and cytochrome b stability
- 2014
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In: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 23:23, s. 6356-6365
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Journal article (peer-reviewed)abstract
- Complex III (cytochrome bc(1)) is a protein complex of the mitochondrial inner membrane that transfers electrons from ubiquinol to cytochrome c. Its assembly requires the coordinated expression of mitochondrial-encoded cytochrome b and nuclear-encoded subunits and assembly factors. Complex III deficiency is a severe multisystem disorder caused by mutations in subunit genes or assembly factors. Sequence-profile-based orthology predicts C11orf83, hereafter named UQCC3, to be the ortholog of the fungal complex III assembly factor CBP4. We describe a homozygous c.59T > A missense mutation in UQCC3 from a consanguineous patient diagnosed with isolated complex III deficiency, displaying lactic acidosis, hypoglycemia, hypotonia and delayed development without dysmorphic features. Patient fibroblasts have reduced complex III activity and lower levels of the holocomplex and its subunits than controls. They have no detectable UQCC3 protein and have lower levels of cytochrome b protein. Furthermore, in patient cells, cytochrome b is absent from a high-molecular-weight complex III. UQCC3 is reduced in cells depleted for the complex III assembly factors UQCC1 and UQCC2. Conversely, absence of UQCC3 in patient cells does not affect UQCC1 and UQCC2. This suggests that UQCC3 functions in the complex III assembly pathway downstream of UQCC1 and UQCC2 and is consistent with what is known about the function of Cbp4 and of the fungal orthologs of UQCC1 and UQCC2, Cbp3 and Cbp6. We conclude that UQCC3 functions in complex III assembly and that the c.59T > A mutation has a causal role in complex III deficiency.
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| 17. |
- Witek, Barbara, et al.
(author)
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Targeted Disruption of ALK Reveals a Potential Role in Hypogonadotropic Hypogonadism
- 2015
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In: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 10:5
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Journal article (peer-reviewed)abstract
- Mice lacking ALK activity have previously been reported to exhibit subtle behavioral phenotypes. In this study of ALK of loss of function mice we present data supporting a role for ALK in hypogonadotropic hypogonadism in male mice. We observed lower level of serum testosterone at P40 in ALK knock-out males, accompanied by mild disorganization of seminiferous tubules exhibiting decreased numbers of GATA4 expressing cells. These observations highlight a role for ALK in testis function and are further supported by experiments in which chemical inhibition of ALK activity with the ALK TKI crizotinib was employed. Oral administration of crizotinib resulted in a decrease of serum testosterone levels in adult wild type male mice, which reverted to normal levels after cessation of treatment. Analysis of GnRH expression in neurons of the hypothalamus revealed a significant decrease in the number of GnRH positive neurons in ALK knock-out mice at P40 when compared with control littermates. Thus, ALK appears to be involved in hypogonadotropic hypogonadism by regulating the timing of pubertal onset and testis function at the upper levels of the hypothalamic-pituitary gonadal axis.
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| 18. |
- Barjesteh van Waalwijk van Doorn-Khosrovani, Sahar, et al.
(author)
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PCM4EU and PRIME-ROSE : Collaboration for implementation of precision cancer medicine in Europe
- 2024
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In: Acta Oncologica. - 1651-226X .- 1651-226X. ; 63, s. 385-391
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Journal article (peer-reviewed)abstract
- BACKGROUND: In the two European Union (EU)-funded projects, PCM4EU (Personalized Cancer Medicine for all EU citizens) and PRIME-ROSE (Precision Cancer Medicine Repurposing System Using Pragmatic Clinical Trials), we aim to facilitate implementation of precision cancer medicine (PCM) in Europe by leveraging the experience from ongoing national initiatives that have already been particularly successful. PATIENTS AND METHODS: PCM4EU and PRIME-ROSE gather 17 and 24 partners, respectively, from 19 European countries. The projects are based on a network of Drug Rediscovery Protocol (DRUP)-like clinical trials that are currently ongoing or soon to start in 11 different countries, and with more trials expected to be established soon. The main aims of both the projects are to improve implementation pathways from molecular diagnostics to treatment, and reimbursement of diagnostics and tumour-tailored therapies to provide examples of best practices for PCM in Europe. RESULTS: PCM4EU and PRIME-ROSE were launched in January and July 2023, respectively. Educational materials, including a podcast series, are already available from the PCM4EU website (http://www.pcm4eu.eu). The first reports, including an overview of requirements for the reimbursement systems in participating countries and a guide on patient involvement, are expected to be published in 2024. CONCLUSION: European collaboration can facilitate the implementation of PCM and thereby provide affordable and equitable access to precision diagnostics and matched therapies for more patients. ble from the PCM4EU website (http://www.pcm4eu.eu). The first reports, including an overview of requirements for the reimbursement systems in participating countries and a guide on patient involvement, are expected to be published in 2024. CONCLUSION: European collaboration can facilitate the implementation of PCM and thereby provide affordable and equitable access to precision diagnostics and matched therapies for more patients.
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