394 research outputs found

    PCNI6: SPECIFIC CHOICES AND EXPENDITURES FOR HERBAL MEDICINES BY CANCER PATIENTS

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    Can sleep be used as an indicator of overreaching and overtraining in athletes?

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    Heales, LJ ORCiD: 0000-0002-4510-3324; Lastella, AM ORCiD: 0000-0003-1793-3811; Sargent, C ORCiD: 0000-0001-5340-4701; Vincent, GE ORCiD: 0000-0002-7036-7823To achieve optimal athletic performance and competition readiness, it is crucial to balance the highest appropriate training stimulus with sufficient recovery. Excessive and/or progressive increases in training load are integral to improving athletic performance (Halson, 2014). However, increased training loads and/or inadequate recovery can result in maladaptation to training, and if continued, can lead to the development of overreaching/overtraining (Meeusen et al., 2013; Cadegiani and Kater, 2017). In terms of recovery, sleep is an essential component of an athlete’s recuperation due to its physiological and psychological restorative effects (Dinges et al., 1997; Pejovic et al., 2013). Sleep quantity and quality declines following augmented increases (+30%) in training load (Hausswirth et al., 2014), and poor sleep is a common complaint among overreached and/or overtrained athletes (Wall et al., 2003). Regardless of whether reduced sleep is a cause or effect of overreaching and/or overtraining, it is possible that measures of sleep could serve as an indicator of the presence of overreaching and/or overtraining. This opinion article will examine the current research underpinning the relationship between insufficient sleep and the development of overreaching/overtraining, describe the implications for practitioners (e.g., sport and exercise scientists, coaches), and identify areas for future research

    The effect of caffeine on subsequent sleep: A systematic review and meta-analysis

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    The consumption of caffeine in response to insufficient sleep may impair the onset and maintenance of subsequent sleep. This systematic review and meta-analysis investigated the effect of caffeine on the characteristics of night-time sleep, with the intent to identify the time after which caffeine should not be consumed prior to bedtime. A systematic search of the literature was undertaken with 24 studies included in the analysis. Caffeine consumption reduced total sleep time by 45 min and sleep efficiency by 7%, with an increase in sleep onset latency of 9 min and wake after sleep onset of 12 min. Duration (+6.1 min) and proportion (+1.7%) of light sleep (N1) increased with caffeine intake and the duration (-11.4 min) and proportion (-1.4%) of deep sleep (N3 and N4) decreased with caffeine intake. To avoid reductions in total sleep time, coffee (107 mg per 250 mL) should be consumed at least 8.8 h prior to bedtime and a standard serve of pre-workout supplement (217.5 mg) should be consumed at least 13.2 h prior to bedtime. The results of the present study provide evidence-based guidance for the appropriate consumption of caffeine to mitigate the deleterious effects on sleep

    Ultrafast changes in lattice symmetry probed by coherent phonons

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    The electronic and structural properties of a material are strongly determined by its symmetry. Changing the symmetry via a photoinduced phase transition offers new ways to manipulate material properties on ultrafast timescales. However, in order to identify when and how fast these phase transitions occur, methods that can probe the symmetry change in the time domain are required. We show that a time-dependent change in the coherent phonon spectrum can probe a change in symmetry of the lattice potential, thus providing an all-optical probe of structural transitions. We examine the photoinduced structural phase transition in VO2 and show that, above the phase transition threshold, photoexcitation completely changes the lattice potential on an ultrafast timescale. The loss of the equilibrium-phase phonon modes occurs promptly, indicating a non-thermal pathway for the photoinduced phase transition, where a strong perturbation to the lattice potential changes its symmetry before ionic rearrangement has occurred.Comment: 14 pages 4 figure

    Inverse Association between trans Isomeric and Long-Chain Polyunsaturated Fatty Acids in Pregnant Women and Their Newborns: Data from Three European Countries

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    Background: trans unsaturated fatty acids are thought to interfere with essential fatty acid metabolism. To extend our knowledge of this phenomenon, we investigated the relationship between trans isomeric and long-chain polyunsaturated fatty acids (LCPUFA) in mothers during pregnancy and in their infants at birth. Methods: Fatty acid composition of erythrocyte phosphatidylcholine (PC) and phosphatidylethanolamine (PE) was determined in Spanish (n = 120), German (n = 78) and Hungarian (n = 43) women at the 20th and 30th week of gestation, at delivery and in their newborns. Results: At the 20th week of gestation, the sum of trans fatty acids in PE was significantly (p < 0.01) lower in Hungarian [0.73 (0.51), % wt/wt, median (IQR)] than in Spanish [1.42 (1.36)] and German [1.30 (1.21)] women. Docosahexaenoic acid (DHA) values in PE were significantly (p < 0.01) higher in Hungarian {[}5.65 (2.09)] than in Spanish [4.37 (2.60)] or German [4.39 (3.3.2)] women. The sum of trans fatty acids significantly inversely correlated to DHA in PCs in Spanish (r = -0.37, p < 0.001), German (n = -0.77, p < 0.001) and Hungarian (r = -0.35, p < 0.05) women, and in PEs in Spanish (r = -0.67, p < 0.001) and German (r = -0.71, p < 0.001), but not in Hungarian (r = -0.02) women. Significant inverse correlations were seen between trans fatty acids and DHA in PEs at the 30th week of gestation (n = 241, r = -0.52, p < 0.001), at delivery (n = 241, r = -0.40, p < 0.001) and in cord lipids (n = 218, r = -0.28, p < 0.001). Conclusion: Because humans cannot synthesize trans isomeric fatty acids, the data obtained in the present study support the concept that high maternal trans isomeric fatty acid intake may interfere with the availability of LCPUFA both for the mother and the fetus. Copyright (C) 2011 S. Karger AG, Base

    Genomic architecture of inflammatory bowel disease in five families with multiple affected individuals.

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    Currently, the best clinical predictor for inflammatory bowel disease (IBD) is family history. Over 163 sequence variants have been associated with IBD in genome-wide association studies, but they have weak effects and explain only a fraction of the observed heritability. It is expected that additional variants contribute to the genomic architecture of IBD, possibly including rare variants with effect sizes larger than the identified common variants. Here we applied a family study design and sequenced 38 individuals from five families, under the hypothesis that families with multiple IBD-affected individuals harbor one or more risk variants that (i) are shared among affected family members, (ii) are rare and (iii) have substantial effect on disease development. Our analysis revealed not only novel candidate risk variants but also high polygenic risk scores for common known risk variants in four out of the five families. Functional analysis of our top novel variant in the remaining family, a rare missense mutation in the ubiquitin ligase TRIM11, suggests that it leads to increased nuclear factor of kappa light chain enhancer in B-cells (NF-κB) signaling. We conclude that an accumulation of common weak-effect variants accounts for the high incidence of IBD in most, but not all families we analyzed and that a family study design can identify novel rare variants conferring risk for IBD with potentially large effect size, such as the TRIM11 p.H414Y mutation

    Distortions of Subjective Time Perception Within and Across Senses

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    Background: The ability to estimate the passage of time is of fundamental importance for perceptual and cognitive processes. One experience of time is the perception of duration, which is not isomorphic to physical duration and can be distorted by a number of factors. Yet, the critical features generating these perceptual shifts in subjective duration are not understood. Methodology/Findings: We used prospective duration judgments within and across sensory modalities to examine the effect of stimulus predictability and feature change on the perception of duration. First, we found robust distortions of perceived duration in auditory, visual and auditory-visual presentations despite the predictability of the feature changes in the stimuli. For example, a looming disc embedded in a series of steady discs led to time dilation, whereas a steady disc embedded in a series of looming discs led to time compression. Second, we addressed whether visual (auditory) inputs could alter the perception of duration of auditory (visual) inputs. When participants were presented with incongruent audio-visual stimuli, the perceived duration of auditory events could be shortened or lengthened by the presence of conflicting visual information; however, the perceived duration of visual events was seldom distorted by the presence of auditory information and was never perceived shorter than their actual durations. Conclusions/Significance: These results support the existence of multisensory interactions in the perception of duration and, importantly, suggest that vision can modify auditory temporal perception in a pure timing task. Insofar as distortions in subjective duration can neither be accounted for by the unpredictability of an auditory, visual or auditory-visual event, we propose that it is the intrinsic features of the stimulus that critically affect subjective time distortions

    Factor structure and validity of the shoulder pain and disability index in a population-based study of people with shoulder symptoms

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    Background: The Shoulder Pain and Disability Index (SPADI) is a self-administered questionnaire that aims to measure pain and disability associated with shoulder disease. The aim of the present study was to investigate the construct validity and factor structure of the SPADI in a population-based study of patients with self-reported chronic shoulder symptoms. Methods: The North West Adelaide Health Study is a representative longitudinal cohort study of people aged 18 years and over. The original sample was randomly selected and recruited by telephone interview. Overall, 3 206 participants returned to the clinic during the second stage (2004-2006) and were asked to report whether they had pain, aching or stiffness on most days in either of their shoulders. Data was also collected on body mass index and shoulder range of motion (ROM) and demographic factors. The SPADI (numeric rating scale) was administered to participants with shoulder symptoms. Principal components factor analysis, with varimax rotation of factor loadings, was used to assess subscale structure of SPADI. Correlations between the SPADI, shoulder ROM and SF-36 were performed. Results: Overall, 22.3% of participants indicated that they had pain, aching or stiffness in either of their shoulders. SPADI results were available for 588 of participants with current shoulder symptoms. The internal consistency of the SPADI subscales were high (Cronbach's alpha > 0.92). Two factors, explaining 61.4% of the total variance were extracted by factor analysis. These were interpreted as disability and pain respectively. There was a strong negative correlation between SPADI disability subscale scores and shoulder range of motion. SPADI disability, but not pain, subscale scores were correlated with age. Conclusions: The SPADI is a valid measure to assess pain and disability in people with shoulder pain in a population-based study. In this setting, the SPADI had a bidimensional structure with both pain and disability subscales.Catherine L Hill, Susan Lester, Anne W Taylor, Michael E Shanahan, Tiffany K Gil

    Identification of a region required for TSC1 stability by functional analysis of TSC1 missense mutations found in individuals with tuberous sclerosis complex

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    Background: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterised by the development of hamartomas in a variety of organs and tissues. The disease is caused by mutations in either the TSC1 gene on chromosome 9q34, or the TSC2 gene on chromosome 16p13.3. The TSC1 and TSC2 gene products, TSC1 and TSC2, form a protein complex that inhibits signal transduction to the downstream effectors of the mammalian target of rapamycin (mTOR). Recently it has been shown that missense mutations to the TSC1 gene can cause TSC. Methods: We have used in vitro biochemical assays to investigate the effects on TSC1 function of TSC1 missense variants submitted to the Leiden Open Variation Database. Results: We identified specific substitutions between amino acids 50 and 190 in the N-terminal region of TSC1 that result in reduced steady state levels of the protein and lead to increased mTOR signalling. Conclusion: Our results suggest that amino acid residues within the N-terminal region of TSC1 are important for TSC1 function and for maintaining the activity of the TSC1-TSC2 complex
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