15 research outputs found

    MicroRNAs in muscle: Characterizing the powerlifter phenotype

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    Powerlifters are the epitome of muscular adaptation and are able to generate extreme forces. The molecular mechanisms underpinning the significant capacity for force generation and hypertrophy are not fully elucidated. MicroRNAs (miRs) are short non-coding RNA sequences that control gene expression via promotion of transcript breakdown and/or translational inhibition. Differences in basal miR expression may partially account for phenotypic differences in muscle mass and function between powerlifters and untrained age-matched controls. Muscle biopsies were obtained from m. vastus lateralis of 15 national level powerlifters (25.1 ± 5.8 years) and 13 untrained controls (24.1 ± 2.0 years). The powerlifters were stronger than the controls (isokinetic knee extension at 60°/s: 307.8 ± 51.6 Nm vs. 211.9 ± 41.9 Nm, respectively P < 0.001), and also had larger muscle fibers (type I CSA 9,122 ± 1,238 vs. 4,511 ± 798 μm2 p < 0.001 and type II CSA 11,100 ± 1,656 vs. 5,468 ± 1,477 μm2 p < 0.001). Of the 17 miRs species analyzed, 12 were differently expressed (p < 0.05) between groups with 7 being more abundant in powerlifters and five having lower expression. Established transcriptionally regulated miR downstream gene targets involved in muscle mass regulation, including myostatin and MyoD, were also differentially expressed between groups. Correlation analysis demonstrates the abundance of eight miRs was correlated to phenotype including peak strength, fiber size, satellite cell abundance, and fiber type regardless of grouping. The unique miR expression profiles between groups allow for categorization of individuals as either powerlifter or healthy controls based on a five miR signature (miR-126, -23b, -16, -23a, -15a) with considerable accuracy (100%). Thus, this unique miR expression may be important to the characterization of the powerlifter phenotype.publishedVersionnivå

    The Slot-Die Coating of Self-Healing Dielectric Materials for the Next Generation of Smart Sensors.

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    Printed electronics (PEs) have attracted a lot of attention over the past decades. The ability to formulate inorganic or organic materials into functional inks with the capacity to be printed onto various substrates presents many advantages, including the capability to be stretchable and conformable, and the potential to be cheaper than current electronics. Therefore, PEs have an enormous promise for enabling novel technologies in a broad range of applications. In a short time, many major advances have been made in this field, including, through the synthesis of conductive polymers, preparation of materials with self-healing properties, and synthesis of stretchable conductors. This project focuses on the printing of a new self-healing dielectric material, previously developed in our group, on a polyethylene terephthalate (PET) substrate through slot-die coating. By paying special attention to environmental impact and compatibility for industrial production, the deposition of this new electroactive material was performed through the control of numerous variables to develop a robust and reliable procedure for the printing of future electronics. Each parameter was individually adjusted, and the resulting films were completely characterized using multiple techniques. This paper will focus on the importance of printed electronics for the development of new technologies, and results from an in-depth characterization will be presented. Moreover, the utilization of the self-healing dielectric materials in fully printed sensors will also be discussed

    Nordiske strategier for medarbeiderdrevet innovasjon – 2013 : Rapport fra arbeidsseminar om medarbeiderdrevet innovasjon (MDI) i Norden

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    Medarbeiderne spiller hovedrollen i nordiske virksomheters innovasjonsarbeid. Medarbeiderdrevet innovasjon (MDI) er en fellesbetegnelse for alle medarbeideres aktive deltagelse i utvikling av varer, tjenester og produksjonsprosesser, arbeidsplassens organisering og knoppskyting fra eksisterende virksomhet. For &#229; fremme medarbeiderdrevet innovasjon i Norden arrangerte Norges formannskap i Nordisk Ministerr&#229;d et arbeidsseminar i Oslo 28. og 29. november 2012. Seminaret samlet eksperter, representanter fra arbeidstaker- og arbeidsgiverorganisasjoner og myndigheter fra Finland, Sverige, Danmark og Norge for &#229; dele erfaringer og dr&#248;fte videre utvikling av MDI som et nordisk konkurransefortrinn. Denne rapporten oppsummerer arbeidet p&#229; seminaret

    Arachidonic acid supplementation transiently augments the acute inflammatory response to resistance exercise in trained men

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    Strenuous exercise can result in skeletal muscle damage, leading to the systemic mobilization, activation and intramuscular accumulation of blood leukocytes. Eicosanoid metabolites of arachidonic acid (ARA) are potent inflammatory mediators, but whether changes in dietary ARA intake influence exercise-induced inflammation is not known. This study investigated the effect of 4 weeks of dietary supplementation with 1.5 g/day ARA (n=9, 24 {plus minus} 1.5 years) or corn-soy oil placebo (n=10, 26 {plus minus} 1.3 years) on systemic and intramuscular inflammatory responses to an acute bout of resistance exercise (8 sets each of leg press and extension at 80% 1RM) in previously trained men. Whole EDTA blood, serum, peripheral blood mononuclear cells (PMBCs), and skeletal muscle biopsies were collected prior to exercise, immediately post-exercise and at 2, 4 and 48 h of recovery. ARA supplementation resulted in higher exercise-stimulated serum creatine kinase activity (incremental area under the curve (iAUC) p=0.046) and blood leukocyte counts (iAUC for total white cells p<0.001, neutrophils p=0.007, monocytes p=0.015). The exercise-induced fold change in PBMC mRNA expression of interleukin-1 beta (IL1B), CD11b (ITGAM) and neutrophil elastase (ELANE), as well as muscle mRNA expression of the chemokines interleukin-8 (CXCL8) and monocyte chemoattractant protein 1 (CCL2) was also greater in the ARA group than placebo. Despite this, ARA supplementation did not influence the histological presence of leukocytes within muscle, perceived muscle soreness or the extent and duration of muscle force loss. These data show that ARA supplementation transiently increased the inflammatory response to acute resistance exercise, but did not impair recovery

    Acute resistance exercise modulates microRNA expression profiles: Combined tissue and circulatory targeted analyses

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    <div><p>A subset of short non-coding RNAs, microRNAs (miRs), have been identified in the regulation of skeletal muscle hypertrophy and atrophy. Expressed within cells, miRs are also present in circulation (c-miR) and have a putative role in cross-tissue signalling. The aim of this study was to examine the impact of a single bout of high intensity resistance exercise (RE) on skeletal muscle and circulatory miRs harvested simultaneously. Resistance trained males (n = 9, 24.6 ± 4.9 years) undertook a single bout of high volume RE with venous blood and muscle biopsies collected before, 2 and 4hr post-exercise. Real time polymerase chain reaction (Rt-PCR) analyses was performed on 30 miRs that have previously been shown to be required for skeletal muscle function. Of these, 6 miRs were significantly altered within muscle following exercise; miR-23a, -133a, -146a, -206, -378b and 486. Analysis of these same miRs in circulation demonstrated minimal alterations with exercise, although c-miR-133a (~4 fold, p = 0.049) and c-miR-149 (~2.4 fold; p = 0.006) were increased 4hr post-exercise. Thus a single bout of RE results in the increased abundance of a subset of miRs within the skeletal muscle, which was not evident in plasma. The lack a qualitative agreement in the response pattern of intramuscular and circulating miR expression suggests the analysis of circulatory miRs is not reflective of the miR responses within skeletal muscle after exercise.</p></div

    c-miR fold change to pre exercise.

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    <p>(<b>A</b>) c-miR-133a and (<b>B</b>) c-miR-149 expression normalized to geomean of 5 endogenous stable miRs (Significant changes from baseline represented as * p≤0.05, ** p<0.01 and *** p<0.001, trends from baseline 0.05</p

    Data-driven Development of ROTEM and TEG Algorithms for the Management of Trauma Hemorrhage:A Prospective Observational Multicenter Study

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    OBJECTIVE: Developing pragmatic data-driven algorithms for management of trauma induced coagulopathy (TIC) during trauma hemorrhage for viscoelastic hemostatic assays (VHAs). BACKGROUND: Admission data from conventional coagulation tests (CCT), rotational thrombelastometry (ROTEM) and thrombelastography (TEG) were collected prospectively at 6 European trauma centers during 2008 to 2013. METHODS: To identify significant VHA parameters capable of detecting TIC (defined as INR > 1.2), hypofibrinogenemia (< 2.0 g/L), and thrombocytopenia (< 100 x10/L), univariate regression models were constructed. Area under the curve (AUC) was calculated, and threshold values for TEG and ROTEM parameters with 70% sensitivity were included in the algorithms. RESULTS: A total of, 2287 adult trauma patients (ROTEM: 2019 and TEG: 968) were enrolled. FIBTEM clot amplitude at 5 minutes (CA5) had the largest AUC and 10 mm detected hypofibrinogenemia with 70% sensitivity. The corresponding value for functional fibrinogen (FF) TEG maximum amplitude (MA) was 19 mm. Thrombocytopenia was similarly detected using the calculated threshold EXTEM-FIBTEM CA5 30 mm. The corresponding rTEG-FF TEG MA was 46 mm. TIC was identified by EXTEM CA5 41 mm, rTEG MA 64 mm (80% sensitivity). For hyperfibrinolysis, we examined the relationship between viscoelastic lysis parameters and clinical outcomes, with resulting threshold values of 85% for EXTEM Li30 and 10% for rTEG Ly30.Based on these analyses, we constructed algorithms for ROTEM, TEG, and CCTs to be used in addition to ratio driven transfusion and tranexamic acid. CONCLUSIONS: We describe a systematic approach to define threshold parameters for ROTEM and TEG. These parameters were incorporated into algorithms to support data-driven adjustments of resuscitation with therapeutics, to optimize damage control resuscitation practice in trauma
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