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- Publication . Article . Other literature type . 2012Open Access EnglishAuthors:Martin J. Gibala; Jonathan P. Little; Maureen J. MacDonald; John A. Hawley;Martin J. Gibala; Jonathan P. Little; Maureen J. MacDonald; John A. Hawley;
pmc: PMC3459051
Publisher: Blackwell Science IncCountry: AustraliaThank you for the opportunity to respond to the letter submitted by Gayda and colleagues in response to our recent review published in The Journal of Physiology (Gibala et al. 2012). With regards to their first comment regarding our new ‘practical’ high-intensity interval exercise (HIIE) protocol, we disagree with the assertion that ‘exercise intensity at 60% of peak power cannot be considered high intensity.’ In our efforts to develop a low-volume HIIE protocol that can be applied across different cohorts including clinical populations, we devised a model comprising 10 × 60 s work bouts at an intensity eliciting ∼85–90% of maximal heart rate (HRmax; averaged over the 10 intervals), interspersed by 60 s of recovery. We have found that the percentage of peak power output (PPO; determined using a standard ramp test to volitional fatigue which does not always elicit peak O2 uptake) that approximates the desired target heart rate (i.e. the % of HRmax) varies considerably between subjects and is exercise-mode specific. For example, in the study by Hood et al. (2011) which was conducted on sedentary healthy adults, a workload equivalent to 60% of PPO during upright cycling was sufficient to elicit a training intensity of ∼90% HRmax. However, in our recent study conducted on patients with type 2 diabetes, the intensity required to elicit ∼90% HRmax was ∼95% of PPO determined during recumbent cycling (Little et al. 2011). We agree with the assertion by Gayda and colleagues that ‘acute physiological responses during different HIIE protocols as well as patient's safety, tolerance and comfort should be tested before their implementation into training programs’. Ongoing protocol optimization work in our laboratory reveal that when interval exercise was prescribed as 80% of PPO in coronary artery disease (CAD) patients – most of whom were taking beta-blocker medication – the 10 × 60 s protocol resulted in peak heart rates during the exercise that averaged ∼85% of age-predicted HRmax. Further, the 10 × 60 s protocol was best tolerated and rated as most preferred by CAD patients in comparison with a modified Wingate protocol (repeated 30 s efforts at 100% PPO with 4 min unloaded cycling for recovery), the standard aerobic interval training protocol used by Wisloff and colleagues (2007), or a moderate-intensity continuous exercise (MICE) protocol. It is likely that high-intensity interval training (HIT) does not conform to a ‘one size fits all’ approach and the interval training stimulus needs to be tailored to individuals depending on their initial level of fitness, exercise tolerance, use of prescription medications and other factors. We also concur with the other main comment by Gayda and colleagues that ‘the superiority of this HIIE protocol [our 10 × 60 s ‘hard’/60 s ‘easy’ model]… needs to be demonstrated.’ Indeed, our review concluded ‘One aspect that is unclear from the present literature is the precise intensity and minimal volume of training that is needed to potentiate the effect of the stimulus-adaptation on outcomes such as mitochondrial biogenesis and relevant health markers. To answer such questions, a complex series of studies needs to be undertaken that systematically ‘titrate’ levels of the ‘training impulse’ and determine subsequent cellular, performance and clinical responses after divergent training interventions.’ Specifically with respect to the use of HIIE in patients with cardiovascular risk or cardiovascular disease, the letter by Gayda and colleagues highlights four references from their laboratory that were not cited in our review. Given the relatively broad scope of our review and the fact that Journal guidelines restricted the number of references to 50, it was obviously not possible to cite all relevant work. Moreover, two of the citations listed by Gayda et al. were acute exercise studies (whereas the focus of our review was training adaptations) and the other two citations were a journal abstract and a recent paper published in February 2012 (neither of which we had access to at the time of submission of our original manuscript). We are also aware of the pioneering research conducted by Meyer and colleagues (e.g. Meyer et al. 1998) and have acknowledged this work in a previous commentary (MacDonald & Currie, 2009). We apologize to all authors whose work on interval training we could not cite due to the broad focus of our review and referencing limitations imposed by The Journal.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2016Open AccessAuthors:Trisha Greenhalgh; Ellen Annandale; Richard Ashcroft; James Barlow; Nick Black; Alan Bleakley; Ruth Boaden; Jeffrey Braithwaite; Nicky Britten; Franco A. Carnevale; +65 moreTrisha Greenhalgh; Ellen Annandale; Richard Ashcroft; James Barlow; Nick Black; Alan Bleakley; Ruth Boaden; Jeffrey Braithwaite; Nicky Britten; Franco A. Carnevale; Katherine Checkland; Julianne Cheek; Alexander M. Clark; Simon Cohn; Jack Coulehan; Benjamin F. Crabtree; Steven Cummins; Frank Davidoff; Huw Davies; Robert Dingwall; Mary Dixon-Woods; Glyn Elwyn; Eivind Engebretsen; Ewan Ferlie; Naomi Fulop; John Gabbay; Marie-Pierre Gagnon; Dariusz Galasiński; Ruth Garside; Lucy Gilson; Peter Griffiths; Penny Hawe; Jan-Kees Helderman; Brian Hodges; David J. Hunter; Margaret H. Kearney; Celia Kitzinger; Jenny Kitzinger; Ayelet Kuper; Saville Kushner; Andrée le May; Lorelei Lingard; Louise Locock; Jill Maben; Mary Ellen Macdonald; Frances S. Mair; Russell Mannion; Martin Marshall; Carl May; Nicholas Mays; Lorna McKee; Marissa Miraldo; David G. Morgan; Janice M. Morse; Sarah Nettleton; Sandy Oliver; Warrren Pearce; Pierre Pluye; Catherine Pope; Glenn Robert; Celia Roberts; Stefania Rodella; Jo Rycroft-Malone; Margarete Sandelowski; Paul G. Shekelle; Fiona Stevenson; Sharon E. Straus; Deborah Swinglehurst; Sally Thorne; Göran Tomson; Gerd Westert; Sue Wilkinson; Brian Williams; Terry Young; Sue Ziebland;Countries: United Kingdom, United Kingdom, Australia, Netherlands, United Kingdom, United Kingdom, United Kingdom, United Kingdom, United Kingdom
Seventy six senior academics from 11 countries invite The BMJ ’s editors to reconsider their policy of rejecting qualitative research on the grounds of low priority. They challenge the journal to develop a proactive, scholarly, and pluralist approach to research that aligns with its stated mission
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You have already added works in your ORCID record related to the merged Research product. - Publication . Other literature type . Article . 2020Open AccessAuthors:Heather L. Petrick; Henver Simionato Brunetta; Chris Pignanelli; Everson Araújo Nunes; Luc J. C. van Loon; Jamie F. Burr; Graham P. Holloway;Heather L. Petrick; Henver Simionato Brunetta; Chris Pignanelli; Everson Araújo Nunes; Luc J. C. van Loon; Jamie F. Burr; Graham P. Holloway;Publisher: WileyCountries: Netherlands, Belgium, AustraliaProject: NSERC
Key points Ketone bodies are proposed to represent an alternative fuel source driving energy production, particularly during exercise. Biologically, the extent to which mitochondria utilize ketone bodies compared to other substrates remains unknown. We demonstratein vitrothat maximal mitochondrial respiration supported by ketone bodies is low when compared to carbohydrate-derived substrates in the left ventricle and red gastrocnemius muscle from rodents, and in human skeletal muscle. When considering intramuscular concentrations of ketone bodies and the presence of other carbohydrate and lipid substrates, biological rates of mitochondrial respiration supported by ketone bodies are predicted to be minimal. At the mitochondrial level, it is therefore unlikely that ketone bodies are an important source for energy production in cardiac and skeletal muscle, particularly when other substrates are readily available. Ketone bodies (KB) have recently gained popularity as an alternative fuel source to support mitochondrial oxidative phosphorylation and enhance exercise performance. However, given the low activity of ketolytic enzymes and potential inhibition from carbohydrate oxidation, it remains unknown if KBs can contribute to energy production. We therefore determined the ability of KBs (sodiumdl-beta-hydroxybutyrate, beta-HB; lithium acetoacetate, AcAc) to stimulatein vitromitochondrial respiration in the left ventricle (LV) and red gastrocnemius (RG) of rats, and in human vastus lateralis. Compared to pyruvate, the ability of KBs to maximally drive respiration was low in isolated mitochondria and permeabilized fibres (PmFb) from the LV (similar to 30-35% of pyruvate), RG (similar to 10-30%), and human vastus lateralis (similar to 2-10%). In PmFb, the concentration of KBs required to half-maximally drive respiration (LV: 889 mu m beta-HB, 801 mu mAcAc; RG: 782 mu m beta-HB, 267 mu mAcAc) were greater than KB content representative of the muscle microenvironment (similar to 100 mu m). This would predict low rates (similar to 1-4% of pyruvate) of biological KB-supported respiration in the LV (8-14 pmol s(-1) mg(-1)) and RG (3-6 pmol s(-1) mg(-1)) at rest and following exercise. Moreover, KBs did not increase respiration in the presence of saturating pyruvate, submaximal pyruvate (100 mu m) reduced the ability of physiological beta-HB to drive respiration, and addition of other intracellular substrates (succinate + palmitoylcarnitine) decreased maximal KB-supported respiration. As a result, product inhibition is likely to limit KB oxidation. Altogether, the ability of KBs to drive mitochondrial respiration is minimal and they are likely to be outcompeted by other substrates, compromising their use as an important energy source.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Other literature type . Article . 2015Open Access EnglishAuthors:Adam L. Bujak; Justin D. Crane; James S. V. Lally; Rebecca J. Ford; Sally J. Kang; Irena A. Rebalka; Alex E. Green; Bruce E. Kemp; Thomas J. Hawke; Jonathan D. Schertzer; +1 moreAdam L. Bujak; Justin D. Crane; James S. V. Lally; Rebecca J. Ford; Sally J. Kang; Irena A. Rebalka; Alex E. Green; Bruce E. Kemp; Thomas J. Hawke; Jonathan D. Schertzer; Gregory R. Steinberg;Publisher: Cell PressCountry: AustraliaProject: NSERC , CIHR
SummaryThe AMP-activated protein kinase (AMPK) activates autophagy, but its role in aging and fasting-induced muscle function has not been defined. Here we report that fasting mice lacking skeletal muscle AMPK (AMPK-MKO) results in hypoglycemia and hyperketosis. This is not due to defective fatty acid oxidation, but instead is related to a block in muscle proteolysis that leads to reduced circulating levels of alanine, an essential amino acid required for gluconeogenesis. Markers of muscle autophagy including phosphorylation of Ulk1 Ser555 and Ser757 and aggregation of RFP-LC3 puncta are impaired. Consistent with impaired autophagy, aged AMPK-MKO mice possess a significant myopathy characterized by reduced muscle function, mitochondrial disease, and accumulation of the autophagy/mitophagy proteins p62 and Parkin. These findings establish an essential requirement for skeletal muscle AMPK-mediated autophagy in preserving blood glucose levels during prolonged fasting as well as maintaining muscle integrity and mitochondrial function during aging.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2015Open AccessAuthors:Margo Mountjoy; Jorunn Sundgot-Borgen; Louise M. Burke; Susan D. Carter; Naama Constantini; Constance M. Lebrun; Nanna L. Meyer; Roberta Sherman; Kathrin Steffen; Richard Budgett; +1 moreMargo Mountjoy; Jorunn Sundgot-Borgen; Louise M. Burke; Susan D. Carter; Naama Constantini; Constance M. Lebrun; Nanna L. Meyer; Roberta Sherman; Kathrin Steffen; Richard Budgett; Arne Ljungqvist;
pmid: 24620037
Country: AustraliaIn April 2014, the International Olympic Committee (IOC) published a Consensus Statement in this journal entitled “Beyond the Female Athlete Triad: Relative Energy Deficiency in Sport (RED-S)”.1 In reference to that Consensus Statement, Professor Mary Jane De Souza and colleagues published an editorial (July 2014).2 The editorial below expands on the original Consensus Statement and comments on the 2014 Editorial by Professor Mary Jane De Souza and colleagues. Albert Einstein said: “The important thing is to never stop questioning.” A group of 11 IOC authors have called attention, as others in the past,3 ,4 to a problem that is wider and more complex than originally identified when the term ‘Female Athlete Triad’ (Triad or FAT) was first coined in 1992. Just as knowledge evolves, so too should ideas and constructs on how to address it. Given the evolution of science since 1992, and to more accurately describe the clinical syndrome originally known as the Female Athlete Triad, the IOC introduced a more comprehensive, broader term: Relative Energy Deficiency in Sport. The syndrome of RED-S refers to impaired physiological functioning caused by relative energy deficiency, and includes but is not limited to impairments of metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health. Our April 2014 Consensus statement identifies the aetiological factor underpinning the syndrome as: an energy deficiency relative to the balance between dietary energy intake and the energy expenditure required to support homeostasis, health and the activities of daily living, growth and sporting activities. We reaffirm the principle that the IOC Consensus Statement highlights about energy deficiency/low energy availability among exercising people. De Souza and colleagues’ editorial criticises the use of the word ‘balance,’ suggesting that the IOC authors have confused the terms energy availability and energy balance. We used the term …
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2011Open AccessAuthors:Hiroko Tanaka; Jessica M. Black; Charles Hulme; Leanne M. Stanley; Shelli R. Kesler; Susan Whitfield-Gabrieli; Allan L. Reiss; John D. E. Gabrieli; Fumiko Hoeft;Hiroko Tanaka; Jessica M. Black; Charles Hulme; Leanne M. Stanley; Shelli R. Kesler; Susan Whitfield-Gabrieli; Allan L. Reiss; John D. E. Gabrieli; Fumiko Hoeft;Country: Australia
Although the role of IQ in developmental dyslexia remains ambiguous, the dominant clinical and research approaches rely on a definition of dyslexia that requires reading skill to be significantly below the level expected given an individual’s IQ. In the study reported here, we used functional MRI (fMRI) to examine whether differences in brain activation during phonological processing that are characteristic of dyslexia were similar or dissimilar in children with poor reading ability who had high IQ scores (discrepant readers) and in children with poor reading ability who had low IQ scores (nondiscrepant readers). In two independent samples including a total of 131 children, using univariate and multivariate pattern analyses, we found that discrepant and nondiscrepant poor readers exhibited similar patterns of reduced activation in brain areas such as left parietotemporal and occipitotemporal regions. These results converge with behavioral evidence indicating that, regardless of IQ, poor readers have similar kinds of reading difficulties in relation to phonological processing.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2010Open Access EnglishAuthors:Frédéric Guay; Julien Chanal; Catherine F. Ratelle; Herbert W. Marsh; Simon Larose; Michel Boivin;Frédéric Guay; Julien Chanal; Catherine F. Ratelle; Herbert W. Marsh; Simon Larose; Michel Boivin;
pmid: 20447334
Countries: United Kingdom, Australia, SwitzerlandBACKGROUND: There are two approaches to the differential examination of school motivation. The first is to examine motivation towards specific school subjects (between school subject differentiation). The second is to examine school motivation as a multidimensional concept that varies in terms of not only intensity but also quality (within school subject differentiation). These two differential approaches have led to important discoveries and provided a better understanding of student motivational dynamics. However, little research has combined these two approaches. AIMS: This study examines young elementary students' motivations across school subjects (writing, reading, and maths) from the stance of self-determination theory. First, we tested whether children self-report different levels of intrinsic, identified, and controlled motivation towards specific school subjects. Second, we verified whether children self-report differentiated types of motivation across school subjects. SAMPLE: Participants were 425 French-Canadian children (225 girls, 200 boys) from three elementary schools. Children were in Grades 1 (N=121), 2 (N=126), and 3 (N=178). RESULTS: Results show that, for a given school subject, young elementary students self-report different levels of intrinsic, identified, and controlled motivation. Results also indicate that children self-report different levels of motivation types across school subjects. Our findings also show that most differentiation effects increase across grades. Some gender effects were also observed. CONCLUSION: These results highlight the importance of distinguishing among types of school motivation towards specific school subjects in the early elementary years.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . 2019Open Access EnglishAuthors:Szabolcs David; Anneriet M. Heemskerk; Francesco Corrivetti; Michel Thiebaut de Schotten; Silvio Sarubbo; Francesco Corsini; Alessandro De Benedictis; Laurent Petit; Max A. Viergever; Derek K. Jones; +5 moreSzabolcs David; Anneriet M. Heemskerk; Francesco Corrivetti; Michel Thiebaut de Schotten; Silvio Sarubbo; Francesco Corsini; Alessandro De Benedictis; Laurent Petit; Max A. Viergever; Derek K. Jones; Emmanuel Mandonnet; Hubertus Axer; John Evans; Tomáš Paus; Alexander Leemans;Publisher: HAL CCSDCountries: France, France, Netherlands, AustraliaProject: WT , NWO | Diffusion MRI analysis be... (25096), NIH | Axon, Testosterone and Me... (5R01MH085772-02)
International audience; Fiber tractography (FT) using diffusion magnetic resonance imaging (dMRI) is widely used for investigating microstructural properties of white matter (WM) fiber-bundles and for mapping structural connections of the human brain. While studying the architectural configuration of the brain's circuitry with FT is not without controversy, recent progress in acquisition, processing, modeling, analysis, and visualization of dMRI data pushes forward the reliability in reconstructing WM pathways. Despite being aware of the well-known pitfalls in analyzing dMRI data and several other limitations of FT discussed in recent literature, we present the superoanterior fasciculus (SAF), a novel bilateral fiber tract in the frontal region of the human brain that-to the best of our knowledge-has not been documented. The SAF has a similar shape to the anterior part of the cingulum bundle, but it is located more frontally. To minimize the possibility that these FT findings are based on acquisition or processing artifacts, different dMRI data sets and processing pipelines have been used to describe the SAF. Furthermore, we evaluated the configuration of the SAF with complementary methods, such as polarized light imaging (PLI) and human brain dissections. The FT results of the SAF demonstrate a long pathway, consistent across individuals, while the human dissections indicate fiber pathways connecting the postero-dorsal with the antero-dorsal cortices of the frontal lobe.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2016Open AccessAuthors:Finnian R. Mc Causland; Brian Claggett; Emmanuel A. Burdmann; Kai-Uwe Eckardt; Reshma Kewalramani; Andrew S. Levey; John J.V. McMurray; Patrick S. Parfrey; Giuseppe Remuzzi; Ajay K. Singh; +3 moreFinnian R. Mc Causland; Brian Claggett; Emmanuel A. Burdmann; Kai-Uwe Eckardt; Reshma Kewalramani; Andrew S. Levey; John J.V. McMurray; Patrick S. Parfrey; Giuseppe Remuzzi; Ajay K. Singh; Scott D. Solomon; Robert D. Toto; Marc A. Pfeffer;Countries: United Kingdom, AustraliaProject: NIH | Cardiac Complications of ... (5K23DK102511-03)
Background:\ud \ud To better understand a potential association of elevated C-reactive protein (CRP) level with progression of chronic kidney disease (CKD), we examined the relationship of CRP level with the development of end-stage renal disease (ESRD) in the Trial to Reduce Cardiovascular Events With Aranesp Therapy (TREAT).\ud \ud Study Design\ud \ud Post hoc analysis of a randomized controlled trial.\ud \ud Setting & Participants:\ud \ud 4,038 patients with type 2 diabetes, CKD, and anemia in TREAT.\ud \ud Predictor:\ud \ud Baseline serum CRP concentrations.\ud \ud Outcomes:\ud \ud The primary outcome was development of ESRD; secondary outcomes included doubling of serum creatinine level, a composite of ESRD/serum creatinine doubling, and a composite of death or ESRD.\ud \ud Measurements:\ud \ud We fit unadjusted and adjusted Cox regression models to test the association of baseline CRP level with time to the development of the outcomes of interest.\ud \ud Results:\ud \ud Mean age of participants was 67 years, 43% were men, and 64% were white. Approximately half (48%) the patients had CRP levels > 3.0 mg/L; 668 patients developed ESRD, and 1,270 developed the composite outcome of death or ESRD. Compared with patients with baseline CRP levels ≤ 3.0 mg/L, those with moderately/markedly elevated CRP levels (≥6.9 mg/L; 24% of patients) had a higher adjusted risk for ESRD (HR, 1.32; 95% CI, 1.07-1.63) and the composite outcome of death or ESRD (HR, 1.41; 95% CI, 1.21-1.64). Although nonsignificant, similar trends were noted in competing-risk models.\ud \ud Limitations:\ud \ud Results may not be generalizable to nondiabetic CKD or diabetic CKD in the absence of anemia.\ud \ud Conclusions:\ud \ud Elevated baseline CRP levels are common in type 2 diabetic patients with anemia and CKD and are associated with the future development of ESRD and the composite of death or ESRD.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2019Open Access EnglishAuthors:Caryl A. Nowson; Karen Lim; Norm R.C. Campbell; Stella L O'Connell; Feng J. He; Robin M. Daly;Caryl A. Nowson; Karen Lim; Norm R.C. Campbell; Stella L O'Connell; Feng J. He; Robin M. Daly;Publisher: Le Jacq Communications, Inc.Country: Australia
The standard for assessing dietary sodium intake is to measure 24-hour urine sodium. On average, 93% of daily sodium intake is excreted over 24-hours. Expense and difficulties in obtaining complete 24-hour collections have led to the measurement of sodium concentration in spot and single-void urine samples, using predictive equations to estimate 24-hour urine sodium. Although multiple predictive equations have been developed, in addition to having an average bias, all the equations overestimate 24-hour sodium at lower levels of 24-hour sodium and underestimate 24-hour urine sodium at higher levels of 24-hour sodium. One of the least biased estimating equations is the INTERSALT equation, which incorporates a spot urine creatinine concentration. The authors hypothesized that differential fractional excretion of sodium (FeNa)(derived from a morning void collection) relative to creatinine would impact on the accuracy of the INTERSALT equation in estimating 24-hour urine sodium. In a prospective study of 139 adults aged 65 years and over, three sequential morning void and 24-hour urine samples were examined. There was a significant correlation between increasing FENa and the difference between estimated and measured 24-hours urine sodium (r = 0.358, P < .01). In the lowest quartile of FENa, the INTERSALT equation overestimated 24-hour urine sodium, but underestimated 24-hour urine sodium with greater magnitude in each of the subsequent quartiles of FENa. Differential excretion of sodium relative to creatinine, potentially impacted by renal blood flow and hydration, among other factors, affected the accuracy of the INTERSALT equation. Additional research may refine the INTERSALT and other predictive equations to increase their accuracy.
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295 Research products, page 1 of 30
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- Publication . Article . Other literature type . 2012Open Access EnglishAuthors:Martin J. Gibala; Jonathan P. Little; Maureen J. MacDonald; John A. Hawley;Martin J. Gibala; Jonathan P. Little; Maureen J. MacDonald; John A. Hawley;
pmc: PMC3459051
Publisher: Blackwell Science IncCountry: AustraliaThank you for the opportunity to respond to the letter submitted by Gayda and colleagues in response to our recent review published in The Journal of Physiology (Gibala et al. 2012). With regards to their first comment regarding our new ‘practical’ high-intensity interval exercise (HIIE) protocol, we disagree with the assertion that ‘exercise intensity at 60% of peak power cannot be considered high intensity.’ In our efforts to develop a low-volume HIIE protocol that can be applied across different cohorts including clinical populations, we devised a model comprising 10 × 60 s work bouts at an intensity eliciting ∼85–90% of maximal heart rate (HRmax; averaged over the 10 intervals), interspersed by 60 s of recovery. We have found that the percentage of peak power output (PPO; determined using a standard ramp test to volitional fatigue which does not always elicit peak O2 uptake) that approximates the desired target heart rate (i.e. the % of HRmax) varies considerably between subjects and is exercise-mode specific. For example, in the study by Hood et al. (2011) which was conducted on sedentary healthy adults, a workload equivalent to 60% of PPO during upright cycling was sufficient to elicit a training intensity of ∼90% HRmax. However, in our recent study conducted on patients with type 2 diabetes, the intensity required to elicit ∼90% HRmax was ∼95% of PPO determined during recumbent cycling (Little et al. 2011). We agree with the assertion by Gayda and colleagues that ‘acute physiological responses during different HIIE protocols as well as patient's safety, tolerance and comfort should be tested before their implementation into training programs’. Ongoing protocol optimization work in our laboratory reveal that when interval exercise was prescribed as 80% of PPO in coronary artery disease (CAD) patients – most of whom were taking beta-blocker medication – the 10 × 60 s protocol resulted in peak heart rates during the exercise that averaged ∼85% of age-predicted HRmax. Further, the 10 × 60 s protocol was best tolerated and rated as most preferred by CAD patients in comparison with a modified Wingate protocol (repeated 30 s efforts at 100% PPO with 4 min unloaded cycling for recovery), the standard aerobic interval training protocol used by Wisloff and colleagues (2007), or a moderate-intensity continuous exercise (MICE) protocol. It is likely that high-intensity interval training (HIT) does not conform to a ‘one size fits all’ approach and the interval training stimulus needs to be tailored to individuals depending on their initial level of fitness, exercise tolerance, use of prescription medications and other factors. We also concur with the other main comment by Gayda and colleagues that ‘the superiority of this HIIE protocol [our 10 × 60 s ‘hard’/60 s ‘easy’ model]… needs to be demonstrated.’ Indeed, our review concluded ‘One aspect that is unclear from the present literature is the precise intensity and minimal volume of training that is needed to potentiate the effect of the stimulus-adaptation on outcomes such as mitochondrial biogenesis and relevant health markers. To answer such questions, a complex series of studies needs to be undertaken that systematically ‘titrate’ levels of the ‘training impulse’ and determine subsequent cellular, performance and clinical responses after divergent training interventions.’ Specifically with respect to the use of HIIE in patients with cardiovascular risk or cardiovascular disease, the letter by Gayda and colleagues highlights four references from their laboratory that were not cited in our review. Given the relatively broad scope of our review and the fact that Journal guidelines restricted the number of references to 50, it was obviously not possible to cite all relevant work. Moreover, two of the citations listed by Gayda et al. were acute exercise studies (whereas the focus of our review was training adaptations) and the other two citations were a journal abstract and a recent paper published in February 2012 (neither of which we had access to at the time of submission of our original manuscript). We are also aware of the pioneering research conducted by Meyer and colleagues (e.g. Meyer et al. 1998) and have acknowledged this work in a previous commentary (MacDonald & Currie, 2009). We apologize to all authors whose work on interval training we could not cite due to the broad focus of our review and referencing limitations imposed by The Journal.
Average popularityAverage popularity In bottom 99%Average influencePopularity: Citation-based measure reflecting the current impact.Average influence In bottom 99%Influence: Citation-based measure reflecting the total impact.add Add to ORCIDPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2016Open AccessAuthors:Trisha Greenhalgh; Ellen Annandale; Richard Ashcroft; James Barlow; Nick Black; Alan Bleakley; Ruth Boaden; Jeffrey Braithwaite; Nicky Britten; Franco A. Carnevale; +65 moreTrisha Greenhalgh; Ellen Annandale; Richard Ashcroft; James Barlow; Nick Black; Alan Bleakley; Ruth Boaden; Jeffrey Braithwaite; Nicky Britten; Franco A. Carnevale; Katherine Checkland; Julianne Cheek; Alexander M. Clark; Simon Cohn; Jack Coulehan; Benjamin F. Crabtree; Steven Cummins; Frank Davidoff; Huw Davies; Robert Dingwall; Mary Dixon-Woods; Glyn Elwyn; Eivind Engebretsen; Ewan Ferlie; Naomi Fulop; John Gabbay; Marie-Pierre Gagnon; Dariusz Galasiński; Ruth Garside; Lucy Gilson; Peter Griffiths; Penny Hawe; Jan-Kees Helderman; Brian Hodges; David J. Hunter; Margaret H. Kearney; Celia Kitzinger; Jenny Kitzinger; Ayelet Kuper; Saville Kushner; Andrée le May; Lorelei Lingard; Louise Locock; Jill Maben; Mary Ellen Macdonald; Frances S. Mair; Russell Mannion; Martin Marshall; Carl May; Nicholas Mays; Lorna McKee; Marissa Miraldo; David G. Morgan; Janice M. Morse; Sarah Nettleton; Sandy Oliver; Warrren Pearce; Pierre Pluye; Catherine Pope; Glenn Robert; Celia Roberts; Stefania Rodella; Jo Rycroft-Malone; Margarete Sandelowski; Paul G. Shekelle; Fiona Stevenson; Sharon E. Straus; Deborah Swinglehurst; Sally Thorne; Göran Tomson; Gerd Westert; Sue Wilkinson; Brian Williams; Terry Young; Sue Ziebland;Countries: United Kingdom, United Kingdom, Australia, Netherlands, United Kingdom, United Kingdom, United Kingdom, United Kingdom, United Kingdom
Seventy six senior academics from 11 countries invite The BMJ ’s editors to reconsider their policy of rejecting qualitative research on the grounds of low priority. They challenge the journal to develop a proactive, scholarly, and pluralist approach to research that aligns with its stated mission
Substantial popularitySubstantial popularity In top 1%Substantial influencePopularity: Citation-based measure reflecting the current impact.Substantial influence In top 1%Influence: Citation-based measure reflecting the total impact.add Add to ORCIDPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product. - Publication . Other literature type . Article . 2020Open AccessAuthors:Heather L. Petrick; Henver Simionato Brunetta; Chris Pignanelli; Everson Araújo Nunes; Luc J. C. van Loon; Jamie F. Burr; Graham P. Holloway;Heather L. Petrick; Henver Simionato Brunetta; Chris Pignanelli; Everson Araújo Nunes; Luc J. C. van Loon; Jamie F. Burr; Graham P. Holloway;Publisher: WileyCountries: Netherlands, Belgium, AustraliaProject: NSERC
Key points Ketone bodies are proposed to represent an alternative fuel source driving energy production, particularly during exercise. Biologically, the extent to which mitochondria utilize ketone bodies compared to other substrates remains unknown. We demonstratein vitrothat maximal mitochondrial respiration supported by ketone bodies is low when compared to carbohydrate-derived substrates in the left ventricle and red gastrocnemius muscle from rodents, and in human skeletal muscle. When considering intramuscular concentrations of ketone bodies and the presence of other carbohydrate and lipid substrates, biological rates of mitochondrial respiration supported by ketone bodies are predicted to be minimal. At the mitochondrial level, it is therefore unlikely that ketone bodies are an important source for energy production in cardiac and skeletal muscle, particularly when other substrates are readily available. Ketone bodies (KB) have recently gained popularity as an alternative fuel source to support mitochondrial oxidative phosphorylation and enhance exercise performance. However, given the low activity of ketolytic enzymes and potential inhibition from carbohydrate oxidation, it remains unknown if KBs can contribute to energy production. We therefore determined the ability of KBs (sodiumdl-beta-hydroxybutyrate, beta-HB; lithium acetoacetate, AcAc) to stimulatein vitromitochondrial respiration in the left ventricle (LV) and red gastrocnemius (RG) of rats, and in human vastus lateralis. Compared to pyruvate, the ability of KBs to maximally drive respiration was low in isolated mitochondria and permeabilized fibres (PmFb) from the LV (similar to 30-35% of pyruvate), RG (similar to 10-30%), and human vastus lateralis (similar to 2-10%). In PmFb, the concentration of KBs required to half-maximally drive respiration (LV: 889 mu m beta-HB, 801 mu mAcAc; RG: 782 mu m beta-HB, 267 mu mAcAc) were greater than KB content representative of the muscle microenvironment (similar to 100 mu m). This would predict low rates (similar to 1-4% of pyruvate) of biological KB-supported respiration in the LV (8-14 pmol s(-1) mg(-1)) and RG (3-6 pmol s(-1) mg(-1)) at rest and following exercise. Moreover, KBs did not increase respiration in the presence of saturating pyruvate, submaximal pyruvate (100 mu m) reduced the ability of physiological beta-HB to drive respiration, and addition of other intracellular substrates (succinate + palmitoylcarnitine) decreased maximal KB-supported respiration. As a result, product inhibition is likely to limit KB oxidation. Altogether, the ability of KBs to drive mitochondrial respiration is minimal and they are likely to be outcompeted by other substrates, compromising their use as an important energy source.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Other literature type . Article . 2015Open Access EnglishAuthors:Adam L. Bujak; Justin D. Crane; James S. V. Lally; Rebecca J. Ford; Sally J. Kang; Irena A. Rebalka; Alex E. Green; Bruce E. Kemp; Thomas J. Hawke; Jonathan D. Schertzer; +1 moreAdam L. Bujak; Justin D. Crane; James S. V. Lally; Rebecca J. Ford; Sally J. Kang; Irena A. Rebalka; Alex E. Green; Bruce E. Kemp; Thomas J. Hawke; Jonathan D. Schertzer; Gregory R. Steinberg;Publisher: Cell PressCountry: AustraliaProject: NSERC , CIHR
SummaryThe AMP-activated protein kinase (AMPK) activates autophagy, but its role in aging and fasting-induced muscle function has not been defined. Here we report that fasting mice lacking skeletal muscle AMPK (AMPK-MKO) results in hypoglycemia and hyperketosis. This is not due to defective fatty acid oxidation, but instead is related to a block in muscle proteolysis that leads to reduced circulating levels of alanine, an essential amino acid required for gluconeogenesis. Markers of muscle autophagy including phosphorylation of Ulk1 Ser555 and Ser757 and aggregation of RFP-LC3 puncta are impaired. Consistent with impaired autophagy, aged AMPK-MKO mice possess a significant myopathy characterized by reduced muscle function, mitochondrial disease, and accumulation of the autophagy/mitophagy proteins p62 and Parkin. These findings establish an essential requirement for skeletal muscle AMPK-mediated autophagy in preserving blood glucose levels during prolonged fasting as well as maintaining muscle integrity and mitochondrial function during aging.
Substantial popularitySubstantial popularity In top 1%Average influencePopularity: Citation-based measure reflecting the current impact.Average influence In bottom 99%Influence: Citation-based measure reflecting the total impact.add Add to ORCIDPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2015Open AccessAuthors:Margo Mountjoy; Jorunn Sundgot-Borgen; Louise M. Burke; Susan D. Carter; Naama Constantini; Constance M. Lebrun; Nanna L. Meyer; Roberta Sherman; Kathrin Steffen; Richard Budgett; +1 moreMargo Mountjoy; Jorunn Sundgot-Borgen; Louise M. Burke; Susan D. Carter; Naama Constantini; Constance M. Lebrun; Nanna L. Meyer; Roberta Sherman; Kathrin Steffen; Richard Budgett; Arne Ljungqvist;
pmid: 24620037
Country: AustraliaIn April 2014, the International Olympic Committee (IOC) published a Consensus Statement in this journal entitled “Beyond the Female Athlete Triad: Relative Energy Deficiency in Sport (RED-S)”.1 In reference to that Consensus Statement, Professor Mary Jane De Souza and colleagues published an editorial (July 2014).2 The editorial below expands on the original Consensus Statement and comments on the 2014 Editorial by Professor Mary Jane De Souza and colleagues. Albert Einstein said: “The important thing is to never stop questioning.” A group of 11 IOC authors have called attention, as others in the past,3 ,4 to a problem that is wider and more complex than originally identified when the term ‘Female Athlete Triad’ (Triad or FAT) was first coined in 1992. Just as knowledge evolves, so too should ideas and constructs on how to address it. Given the evolution of science since 1992, and to more accurately describe the clinical syndrome originally known as the Female Athlete Triad, the IOC introduced a more comprehensive, broader term: Relative Energy Deficiency in Sport. The syndrome of RED-S refers to impaired physiological functioning caused by relative energy deficiency, and includes but is not limited to impairments of metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health. Our April 2014 Consensus statement identifies the aetiological factor underpinning the syndrome as: an energy deficiency relative to the balance between dietary energy intake and the energy expenditure required to support homeostasis, health and the activities of daily living, growth and sporting activities. We reaffirm the principle that the IOC Consensus Statement highlights about energy deficiency/low energy availability among exercising people. De Souza and colleagues’ editorial criticises the use of the word ‘balance,’ suggesting that the IOC authors have confused the terms energy availability and energy balance. We used the term …
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2011Open AccessAuthors:Hiroko Tanaka; Jessica M. Black; Charles Hulme; Leanne M. Stanley; Shelli R. Kesler; Susan Whitfield-Gabrieli; Allan L. Reiss; John D. E. Gabrieli; Fumiko Hoeft;Hiroko Tanaka; Jessica M. Black; Charles Hulme; Leanne M. Stanley; Shelli R. Kesler; Susan Whitfield-Gabrieli; Allan L. Reiss; John D. E. Gabrieli; Fumiko Hoeft;Country: Australia
Although the role of IQ in developmental dyslexia remains ambiguous, the dominant clinical and research approaches rely on a definition of dyslexia that requires reading skill to be significantly below the level expected given an individual’s IQ. In the study reported here, we used functional MRI (fMRI) to examine whether differences in brain activation during phonological processing that are characteristic of dyslexia were similar or dissimilar in children with poor reading ability who had high IQ scores (discrepant readers) and in children with poor reading ability who had low IQ scores (nondiscrepant readers). In two independent samples including a total of 131 children, using univariate and multivariate pattern analyses, we found that discrepant and nondiscrepant poor readers exhibited similar patterns of reduced activation in brain areas such as left parietotemporal and occipitotemporal regions. These results converge with behavioral evidence indicating that, regardless of IQ, poor readers have similar kinds of reading difficulties in relation to phonological processing.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2010Open Access EnglishAuthors:Frédéric Guay; Julien Chanal; Catherine F. Ratelle; Herbert W. Marsh; Simon Larose; Michel Boivin;Frédéric Guay; Julien Chanal; Catherine F. Ratelle; Herbert W. Marsh; Simon Larose; Michel Boivin;
pmid: 20447334
Countries: United Kingdom, Australia, SwitzerlandBACKGROUND: There are two approaches to the differential examination of school motivation. The first is to examine motivation towards specific school subjects (between school subject differentiation). The second is to examine school motivation as a multidimensional concept that varies in terms of not only intensity but also quality (within school subject differentiation). These two differential approaches have led to important discoveries and provided a better understanding of student motivational dynamics. However, little research has combined these two approaches. AIMS: This study examines young elementary students' motivations across school subjects (writing, reading, and maths) from the stance of self-determination theory. First, we tested whether children self-report different levels of intrinsic, identified, and controlled motivation towards specific school subjects. Second, we verified whether children self-report differentiated types of motivation across school subjects. SAMPLE: Participants were 425 French-Canadian children (225 girls, 200 boys) from three elementary schools. Children were in Grades 1 (N=121), 2 (N=126), and 3 (N=178). RESULTS: Results show that, for a given school subject, young elementary students self-report different levels of intrinsic, identified, and controlled motivation. Results also indicate that children self-report different levels of motivation types across school subjects. Our findings also show that most differentiation effects increase across grades. Some gender effects were also observed. CONCLUSION: These results highlight the importance of distinguishing among types of school motivation towards specific school subjects in the early elementary years.
Substantial popularitySubstantial popularity In top 1%Substantial influencePopularity: Citation-based measure reflecting the current impact.Substantial influence In top 1%Influence: Citation-based measure reflecting the total impact.add Add to ORCIDPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product. - Publication . Article . 2019Open Access EnglishAuthors:Szabolcs David; Anneriet M. Heemskerk; Francesco Corrivetti; Michel Thiebaut de Schotten; Silvio Sarubbo; Francesco Corsini; Alessandro De Benedictis; Laurent Petit; Max A. Viergever; Derek K. Jones; +5 moreSzabolcs David; Anneriet M. Heemskerk; Francesco Corrivetti; Michel Thiebaut de Schotten; Silvio Sarubbo; Francesco Corsini; Alessandro De Benedictis; Laurent Petit; Max A. Viergever; Derek K. Jones; Emmanuel Mandonnet; Hubertus Axer; John Evans; Tomáš Paus; Alexander Leemans;Publisher: HAL CCSDCountries: France, France, Netherlands, AustraliaProject: WT , NWO | Diffusion MRI analysis be... (25096), NIH | Axon, Testosterone and Me... (5R01MH085772-02)
International audience; Fiber tractography (FT) using diffusion magnetic resonance imaging (dMRI) is widely used for investigating microstructural properties of white matter (WM) fiber-bundles and for mapping structural connections of the human brain. While studying the architectural configuration of the brain's circuitry with FT is not without controversy, recent progress in acquisition, processing, modeling, analysis, and visualization of dMRI data pushes forward the reliability in reconstructing WM pathways. Despite being aware of the well-known pitfalls in analyzing dMRI data and several other limitations of FT discussed in recent literature, we present the superoanterior fasciculus (SAF), a novel bilateral fiber tract in the frontal region of the human brain that-to the best of our knowledge-has not been documented. The SAF has a similar shape to the anterior part of the cingulum bundle, but it is located more frontally. To minimize the possibility that these FT findings are based on acquisition or processing artifacts, different dMRI data sets and processing pipelines have been used to describe the SAF. Furthermore, we evaluated the configuration of the SAF with complementary methods, such as polarized light imaging (PLI) and human brain dissections. The FT results of the SAF demonstrate a long pathway, consistent across individuals, while the human dissections indicate fiber pathways connecting the postero-dorsal with the antero-dorsal cortices of the frontal lobe.
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You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2016Open AccessAuthors:Finnian R. Mc Causland; Brian Claggett; Emmanuel A. Burdmann; Kai-Uwe Eckardt; Reshma Kewalramani; Andrew S. Levey; John J.V. McMurray; Patrick S. Parfrey; Giuseppe Remuzzi; Ajay K. Singh; +3 moreFinnian R. Mc Causland; Brian Claggett; Emmanuel A. Burdmann; Kai-Uwe Eckardt; Reshma Kewalramani; Andrew S. Levey; John J.V. McMurray; Patrick S. Parfrey; Giuseppe Remuzzi; Ajay K. Singh; Scott D. Solomon; Robert D. Toto; Marc A. Pfeffer;Countries: United Kingdom, AustraliaProject: NIH | Cardiac Complications of ... (5K23DK102511-03)
Background:\ud \ud To better understand a potential association of elevated C-reactive protein (CRP) level with progression of chronic kidney disease (CKD), we examined the relationship of CRP level with the development of end-stage renal disease (ESRD) in the Trial to Reduce Cardiovascular Events With Aranesp Therapy (TREAT).\ud \ud Study Design\ud \ud Post hoc analysis of a randomized controlled trial.\ud \ud Setting & Participants:\ud \ud 4,038 patients with type 2 diabetes, CKD, and anemia in TREAT.\ud \ud Predictor:\ud \ud Baseline serum CRP concentrations.\ud \ud Outcomes:\ud \ud The primary outcome was development of ESRD; secondary outcomes included doubling of serum creatinine level, a composite of ESRD/serum creatinine doubling, and a composite of death or ESRD.\ud \ud Measurements:\ud \ud We fit unadjusted and adjusted Cox regression models to test the association of baseline CRP level with time to the development of the outcomes of interest.\ud \ud Results:\ud \ud Mean age of participants was 67 years, 43% were men, and 64% were white. Approximately half (48%) the patients had CRP levels > 3.0 mg/L; 668 patients developed ESRD, and 1,270 developed the composite outcome of death or ESRD. Compared with patients with baseline CRP levels ≤ 3.0 mg/L, those with moderately/markedly elevated CRP levels (≥6.9 mg/L; 24% of patients) had a higher adjusted risk for ESRD (HR, 1.32; 95% CI, 1.07-1.63) and the composite outcome of death or ESRD (HR, 1.41; 95% CI, 1.21-1.64). Although nonsignificant, similar trends were noted in competing-risk models.\ud \ud Limitations:\ud \ud Results may not be generalizable to nondiabetic CKD or diabetic CKD in the absence of anemia.\ud \ud Conclusions:\ud \ud Elevated baseline CRP levels are common in type 2 diabetic patients with anemia and CKD and are associated with the future development of ESRD and the composite of death or ESRD.
Average popularityAverage popularity In bottom 99%Average influencePopularity: Citation-based measure reflecting the current impact.Average influence In bottom 99%Influence: Citation-based measure reflecting the total impact.add Add to ORCIDPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product. - Publication . Article . Other literature type . 2019Open Access EnglishAuthors:Caryl A. Nowson; Karen Lim; Norm R.C. Campbell; Stella L O'Connell; Feng J. He; Robin M. Daly;Caryl A. Nowson; Karen Lim; Norm R.C. Campbell; Stella L O'Connell; Feng J. He; Robin M. Daly;Publisher: Le Jacq Communications, Inc.Country: Australia
The standard for assessing dietary sodium intake is to measure 24-hour urine sodium. On average, 93% of daily sodium intake is excreted over 24-hours. Expense and difficulties in obtaining complete 24-hour collections have led to the measurement of sodium concentration in spot and single-void urine samples, using predictive equations to estimate 24-hour urine sodium. Although multiple predictive equations have been developed, in addition to having an average bias, all the equations overestimate 24-hour sodium at lower levels of 24-hour sodium and underestimate 24-hour urine sodium at higher levels of 24-hour sodium. One of the least biased estimating equations is the INTERSALT equation, which incorporates a spot urine creatinine concentration. The authors hypothesized that differential fractional excretion of sodium (FeNa)(derived from a morning void collection) relative to creatinine would impact on the accuracy of the INTERSALT equation in estimating 24-hour urine sodium. In a prospective study of 139 adults aged 65 years and over, three sequential morning void and 24-hour urine samples were examined. There was a significant correlation between increasing FENa and the difference between estimated and measured 24-hours urine sodium (r = 0.358, P < .01). In the lowest quartile of FENa, the INTERSALT equation overestimated 24-hour urine sodium, but underestimated 24-hour urine sodium with greater magnitude in each of the subsequent quartiles of FENa. Differential excretion of sodium relative to creatinine, potentially impacted by renal blood flow and hydration, among other factors, affected the accuracy of the INTERSALT equation. Additional research may refine the INTERSALT and other predictive equations to increase their accuracy.
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