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{"references": ["A. M. Mathai, The concept of correlation and misinterpretations. International\nJournal of Mathematical and Statistical Sciences, 1998, 7: 157-167.", "R. A. Fisher, Distribution of the values of the correlation coefficient in\nsamples from an indefinitely large population. Biometrika, 1915, 10: 507-\n521.", "A. Winterbottom, A note on the derivation of Fisher-s transformation of\nthe correlation coefficient. The American Statistician, 1979, 33: 142-143.", "H. Hotelling, New light on the correlation coefficient and its transforms.\nJournal of Royal Statistical Society, Ser. B., 1953, 15: 193-232.", "A. K. Gayen, The frequency distribution of the product-moment correlation\ncoefficient in random samples of any size drawn from non-normal\nuniverses. Biometrika, 1951, 38: 219-247.", "D. L. Hawkins, Using U statistics to derive the asymptotic distribution\nof Fisher-s Z statistic. The American Statistician, 1989, 43: 235-237.", "S. Konishi, An approximation to the distribution of the sample correlation\ncoefficient. Biometrika, 1978, 65: 654-656.", "H.-T. Ha and S. B. Provost, A viable alternative to resorting to statistical\ntables. Communications in Statistics-Simulation and Computation, 2007,\n36: 1135-1151."]} Given a bivariate normal sample of correlated variables, (Xi, Yi), i = 1, . . . , n, an alternative estimator of Pearson's correlation coefficient is obtained in terms of the ranges, |Xi − Yi|. An approximate confidence interval for ρX,Y is then derived, and a simulation study reveals that the resulting coverage probabilities are in close agreement with the set confidence levels. As well, a new approximant is provided for the density function of R, the sample correlation coefficient. A mixture involving the proposed approximate density of R, denoted by hR(r), and a density function determined from a known approximation due to R. A. Fisher is shown to accurately approximate the distribution of R. Finally, nearly exact density approximants are obtained on adjusting hR(r) by a 7th degree polynomial.

The former genera Oncocnemis Lederer, Apharetra Grote, Hemistilbia Barnes and Benjamin, Adita Grote, Lepipolys Guenée, Homoncocnemis Hampson, and Homohadena Grote are synonymized under Sympistis Hübner. The following are transferred from Oxycnemis Grote to Sympistis: Sympistis franclemonti (Blanchard), comb. n. [Oxycnemis franclemonti Blanchard] and Sympistis subsimplex (Dyar) comb. n. [Oxycnemis subsimplex Dyar]. Two species are transferred to Unciella gen. n. as Unciella primula (Barnes and McDunnough) comb. n. [Oncocnemis primula Barnes and McDunnough] and Unciella flagrantis (Smith) comb. n. [Oncocnemis flagrantis Smith], which along with Leucocnemis Hampson are transferred to tribe Triocnemidini in the Psaphidinae. Supralathosea Barnes and Benjamin is transferred to Psaphidinae: Psaphidini and Catabena pronuba Barnes and McDunnough is transferred to Supralathosea comb. n.. In addition, Cerapoda Smith syn. n. and Prochloridea Barnes and McDunnough syn. n. (Prochloridea is presently in Hodges “unassociated genera”) are synonymized under Rhizagrotis Smith in the Xyleninae. Copanarta sexpunctata Barnes and McDunnough rev. comb. is transferred from Stylopoda to Copanarta. Oncocnemis simplicia Smith syn. n. is synonymized under Homohadena deserta Smith, Oncocnemis mus Troubridge and Crabo syn. n. under Oncocnemis tenuifascia Smith, and Oncocnemis sala Mustelin syn. n. under Oncocnemis aqualis Grote. The following are elevated to species rank: Sympistis deserticola (McDunnough) stat. n., comb. n. [Oncocnemis riparia deserticola McDunnough], Sympistis pallidior (Barnes) stat. n., comb. n. [Oncocnemis figurata pallidior Barnes] and Sympistis pallida (Barnes) stat. n., comb. n. [Oncocnemis homogena pallida Barnes]. The following 50 species are described as new: Sympistis acheron Troubridge, Sympistis amenthes Troubridge, Sympistis amun Troubridge, Sympistis anubis Troubridge, Sympistis anweileri Troubridge and Lafontaine, Sympistis apep Troubridge, Sympistis apis Troubridge, Sympistis babi Troubridge, Sympistis baloghi Troubridge, Sympistis bes Troubridge, Sympistis buchis Troubridge, Sympistis buto Troubridge, Sympistis cherti Troubridge, Sympistis chons Troubridge, Sympistis cleopatra Troubridge, Sympistis cocytus Troubridge, Sympistis collaris Troubridge, Sympistis dischorda Troubridge, Sympistis disfigurata Troubridge, Sympistis doris Dimock and Troubridge, Sympistis hapi Troubridge, Sympistis hathor Troubridge, Sympistis horus Troubridge, Sympistis incubus Troubridge, Sympistis insanina Troubridge, Sympistis isis Troubridge, Sympistis jenniferae Troubridge, Sympistis jocelynae Troubridge, Sympistis khem Troubridge, Sympistis khepri Troubridge, Sympistis knudsoni Troubridge, Sympistis lachrymosa Troubridge, Sympistis min Troubridge, Sympistis mut Troubridge, Sympistis nenun Troubridge, Sympistis opleri Troubridge, Sympistis osiris Troubridge, Sympistis pachet Troubridge, Sympistis ptah Troubridge, Sympistis ra Troubridge, Sympistis richersi Troubridge, Sympistis sakhmet Troubridge, Sympistis septu Troubridge, Sympistis sesmu Troubridge, Sympistis seth Troubridge, Sympistis shait Troubridge, Sympistis shirleyae Troubridge, Sympistis sobek Troubridge, Sympistis sokar Troubridge, and Sympistis serapis Troubridge. Color illustrations are provided for adults of all nearctic Sympistis species. Alphabetical and phylogenetic checklists of North American Oncocnemidinae are also provided, including species formerly placed there, but here transferred to other subfamilies.

We present in this paper a useful strategy to solve stochastic partial differential equations (SPDEs) involving stochastic coefficients. Using the Wick-product of higher order and the Wiener-Itˆo chaos expansion, the SPDEs is reformulated as a large system of deterministic partial differential equations. To reduce the computational complexity of this system, we shall use a decomposition-coordination method. To obtain the chaos coefficients in the corresponding deterministic equations, we use a least square formulation. Once this approximation is performed, the statistics of the numerical solution can be easily evaluated.

Thank 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.

Key pointsKetone 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.

This deliverable describes the organisation, results and validation phase of the second Gender STI Co-Design Lab (hereafter the Lab) involving participants from America and Europe. The Co-design Lab that took place between October and November 2022 addressed the Gender STI objectives to integrate the gender perspective in bilateral and multilateral agreements between the EU Member States (MS), Associated Countries (AC) and third countries through design thinking methods and participatory techniques. The document describes the methods, participatory steps and tools that have been applied in the Lab to co-design shared solutions and prototypes for common challenges regarding gender inequalities in STI and to support the emergence of an international community of practitioners with similar challenging objectives. More specifically, the deliverable collects in detail “what” was done and how it was done in the Lab, reflects on the “so what” question, as to the sense and purpose of the challenge-based prototypes and their initial outputs, and finally draws some conclusions with a “now what” reflection on what was learnt and suggests possible priorities for future actions.

Aims Treatment of patients with heart failure (HF) relies on measurement of LVEF. However, the extent to which EF is recorded varies markedly. We sought to characterize the patient group that is missing a measure of EF, and to explore the association between missing EF and outcome. Methods and results Individual data on 30 445 patients from 28 observational studies in the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) project were used to compare the prevalence of co-morbidities and outcome across three groups of HF patients: those with missing EF (HF-mEF), reduced EF (HF-REF), and preserved EF (HF-PEF). A total of 29% had HF-mEF, 52% HF-REF, and 19% HF-PEF. Compared with patients in whom EF was known, patients with HF-mEF were older, had a greater prevalence of COPD and previous stroke, and were smokers. Patients with HF-mEF were less likely to receive evidence-based treatment than those with HF-REF. Adjusted mortality in HF-mEF was similar to that in HF-REF and greater than that in HF-PEF at 3 years [HF-REF, hazard ratio (HR) 1.03, 95% confidence interval (CI) 0.95–1.12); HF-PEF, HR 0.78, 95% CI 0.71–0.86]. Conclusion Missing EF is common. The short- and long-term outcome of patients with HF-mEF is poor and they exhibit different co-morbidity profiles and treatment patterns compared with patients with known EF. HF patients with missing EF represent a high risk group.

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This study investigated, in on-reserve First Nations (FN) youth in Ontario, Canada, the following: (a) the intakes of vegetable and fruit, “other” foods and relevant nutrients as compared to current recommendations and national averages, (b) current prevalence rates of overweight and obesity and (c) the relationship between latitude and dietary intakes. Twenty-four-hour diet recalls were collected via the Waterloo Web-Based Eating Behaviour Questionnaire (WEB-Q) (n = 443). Heights and weights of participants were self reported using measured values and Body Mass Index was categorized using the International Obesity Task Force cutoffs. Food group and nutrient intakes were compared to current standards, Southern Ontario Food Behaviour data and the Canadian Community Health Survey, Cycle 2.2, using descriptive statistics. Mean vegetable and fruit, fibre and folate intakes were less than current recommendations. Girls aged 14–18 years had mean intakes of vitamin A below current recommendations for this sub-group; for all sub-groups, mean intakes of vegetables and fruit were below Canadian averages. All sub-groups also had intakes of all nutrients and food groups investigated that were less than those observed in non-FN youth from Southern Ontario, with the exception of “other” foods in boys 12–18 years. Prevalence rates of overweight and obesity were 31.8% and 19.6%, respectively, exceeding rates in the general population. Dietary intakes did not vary consistently by latitude (n = 248), as revealed by ANOVA. This study provided a unique investigation of the dietary intakes of on-reserve FN youth in Ontario and revealed poor intakes of vegetables and fruit and related nutrients and high intakes of “other” foods. Prevalence rates of overweight and obesity exceed those of the general population.

The capacity to focus one's attention for an extended period of time can be increased through training in contemplative practices. However, the cognitive processes engaged during meditation that support trait changes in cognition are not well characterized. We conducted a longitudinal wait-list controlled study of intensive meditation training. Retreat participants practiced focused attention (FA) meditation techniques for three months during an initial retreat. Wait-list participants later undertook formally identical training during a second retreat. Dense-array scalp-recorded electroencephalogram (EEG) data were collected during 6 min of mindfulness of breathing meditation at three assessment points during each retreat. Second-order blind source separation, along with a novel semi-automatic artifact removal tool (SMART), was used for data preprocessing. We observed replicable reductions in meditative state-related beta-band power bilaterally over anteriocentral and posterior scalp regions. In addition, individual alpha frequency (IAF) decreased across both retreats and in direct relation to the amount of meditative practice. These findings provide evidence for replicable longitudinal changes in brain oscillatory activity during meditation and increase our understanding of the cortical processes engaged during meditation that may support long-term improvements in cognition.