504 research outputs found

    Injustice perceptions about pain: parent–child discordance is associated with worse functional outcomes

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    Pain is experienced within and influenced by social environments. For children with chronic pain, the child–parent relationship and parental beliefs about pain are particularly important and may influence pain outcomes. Pain-related injustice perceptions have recently been identified as an important cognitive–emotional factor for children with pain. The current study aimed to better understand the pain-related injustice perceptions of children with chronic pain and their parents. The sample consisted of 253 pediatric chronic pain patients (mean age = 14.1 years, 74% female) presenting to a tertiary pain clinic. Patients completed measures of pain intensity, pain-related injustice perceptions, stress, functional disability, and quality of life. Parents completed a measure of pain-related injustice perceptions about their child's pain. Child–parent dyads were categorized into 1 of 4 categories based on the degree of concordance or discordance between their scores on the injustice measures. One-way analysis of variances examined differences in pain intensity, stress, functional disability, and quality of life across the 4 dyad categories. Our findings indicated that both the degree (concordant vs discordant) and direction (discordant low child–high parent vs discordant high child–low parent) of similarity between child and parent injustice perceptions were associated with child-reported pain intensity, stress, functional disability, and quality of life. The poorest outcomes were reported when children considered their pain as highly unjust, but their parents did not. These findings highlight the important role of parents in the context of pain-related injustice perceptions in pediatric chronic pain

    (Dis)Agreement in Parent-Child Perceptions of Injustice and Their Relationship to Pain Outcomes

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    poster abstractPerceiving one’s pain as unjust and thinking about pain in a catastrophic manner are linked to worse outcomes in children with chronic pain. Dyads where the child catastrophized more than the parent experienced particularly poor outcomes in previous research. We investigated the concordance between parent and child injustice perceptions and its relationship to pain outcomes. 139 patients (age=15.4±2.1; 71.9% female) attending the pain clinic at Riley Children’s Hospital completed measures of perceived injustice, pain, and QOL. Parents completed a measure of perceived injustice about their child’s pain. Parent-child dyads were categorized into one of four groups based on concordance of injustice perceptions: (1) concordant high, (2) concordant low, (3) discordant high parent (P) – low child (C), and (4) discordant low P – high C. Parent injustice perceptions were significantly higher than child perceptions (t(138)=5.80, p<.001, d=.50). ANOVAs identified significant group differences for pain intensity (F(3,138)=2.80, p<.05, η2=.06) and QOL (F(3,138)=15.11, p<.01, η2=.25). For pain intensity, discordant low P – high C dyads reported the highest pain, and significantly higher pain than discordant high P – low C dyads (mean difference [MD]=1.94, p<.05). Concordant high dyads reported the second highest pain. A similar pattern emerged for QOL. Discordant low P – high C dyads reported the worst QOL, and significantly worse QOL than concordant high dyads (MD=-10.22, p<.01), concordant low dyads (MD=-23.70, p<.01), and discordant high P – low C dyads (MD=-28.97, p<.01). Concordant high dyads reported the second worse QOL. Overall, dyads where the child endorsed high injustice perceptions, regardless of parental perceptions, experienced worse pain and QOL, with the worst outcomes observed for discordant dyads (low P – high C). Children in low P – high C dyads may feel invalidated and, thus, use maladaptive strategies in an attempt to communicate the severity of their pain. Research is needed to identify the mechanisms underlying these relationships

    Evidence that heat acclimation training may alter sleep and incidental activity

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    This randomized cross-over study tested the hypothesis that heat acclimation training would detrimentally affect sleep variables and alter incidental physical activity compared to a thermoneutral training control condition. Eight recreationally trained males (V̇ O2peak 49±4.9 mL. kg-1.min-1) completed two separate interventions separated by at least 31 days: 5 consecutive day training blocks of moderate-intensity cycling (60 min·day-1 at 50% peak power output) in a hot (34.9±0.7 °C and 53±4 % relative humidity) and a temperate (22.2±2.6 °C; 65±8 % relative humidity) environment. Wrist-mounted accelerometers were worn continuously for the length of the training blocks and recorded physical activity, sleep quality and quantity. Data were analysed in a Bayesian framework, with the results presented as the posterior probability that a coefficient was greater or less than zero. Compared to the temperate training environment, heat acclimation impaired sleep efficiency (Pr β0 = .917). Daily sedentary time was, on average, 35 min longer (Pr β>0 = .973) and light physical activity time 18 min shorter (Pr β>0 = .960) during the heat acclimation period. No differences were observed between conditions in sleep duration, subjective sleep quality, or moderate or vigorous physical activity. These findings may suggest that athletes and coaches need to be cognisant that heat acclimation training may alter sleep quality and increase sedentary behaviour

    What about the partner? -factors associated with patient-perceived partner dyspareunia in men with Peyronie\u27s disease

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    Background: Limited data are available on how partners of men with Peyronie\u27s disease (PD) are affected by the disease. We sought to characterize PD patients whose curvatures result in pain for their partners during penetrative intercourse. Methods: We queried a database of all men undergoing initial evaluation for PD at a single clinic between March 2014 and June 2016. Patients were administered a questionnaire regarding sexual health concerns with domains including erectile dysfunction, ejaculatory dysfunction, libido, and penile curvature. In the penile curvature section, patients were specifically asked: Does the curvature cause your partner any pain during penetrative intercourse? (Y/N). Patients\u27 partners were not directly evaluated for conditions associated with dyspareunia. Additionally, patients interested in treatment for PD underwent objective curve assessment after intracavernosal injection of erectogenic medications along with penile duplex Doppler ultrasound. Statistical analysis was performed to identify differences in clinicopathologic variables and patient-responses to questionnaire prompts between patients who did and did not report partner pain with intercourse. Results: A total of 322 patients with information available on partner pain were included in the study. Patients who reported partner pain had significantly higher subjective erectile rigidity (mean 5.9/10 Conclusions: Men with superior erectile function, higher degrees of penile curvature and ventral curvatures were more likely to report partner pain during penetrative intercourse. These specific disease characteristics reported in this series may assist clinicians in identifying men who are more motivated to select more invasive therapies

    Parallelism and divergence in immune responses: a comparison of expression levels in two lakes

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    Question: How do immune phenotypes differ between infected and uninfected wild individuals, and is the effect the same in different populations? Organisms: Threespine stickleback (Gasterosteus aculeatus) from two lake populations on the island of North Uist, Scotland, sampled in May 2015. Methods: For each fish, we recorded length, sex, reproductive status, condition, and parasitic infection. We measured the expression levels of eight genes that act as key markers of immune system function using qPCR, and then examined the relationship between measured factors and immune gene expression profiles within each population. Conclusions: Populations differed significantly in their immune gene expression profiles. Within each population, multiple factors, including condition, reproductive status, and Schistocephalus solidus infection levels, were found to correlate with expression levels of different arms of the immune system

    Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise.

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    Sprint interval exercise improves several health markers but the appetite and energy balance response is unknown. This study compared the effects of sprint interval and endurance exercise on appetite, energy intake and gut hormone responses. Twelve healthy males [mean (SD): age 23 (3) years, body mass index 24.2 (2.9) kg m(-2), maximum oxygen uptake 46.3 (10.2) mL kg(-1) min(-1)] completed three 8 h trials [control (CON), endurance exercise (END), sprint interval exercise (SIE)] separated by 1 week. Trials commenced upon completion of a standardised breakfast. Sixty minutes of cycling at 68.1 (4.3) % of maximum oxygen uptake was performed from 1.75-2.75 h in END. Six 30-s Wingate tests were performed from 2.25-2.75 h in SIE. Appetite ratings, acylated ghrelin and peptide YY (PYY) concentrations were measured throughout each trial. Food intake was monitored from buffet meals at 3.5 and 7 h and an overnight food bag. Appetite (P 0.05). Therefore, relative energy intake (energy intake minus the net energy expenditure of exercise) was lower in END than that in CON (15.7 %; P = 0.006) and SIE (11.5 %; P = 0.082). An acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise

    The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy

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    AbstractUsing confocal microscopy, onset of the mitochondrial permeability transition (MPT) in individual mitochondria within living cells can be visualized by the redistribution of the cytosolic fluorophore, calcein, into mitochondria. Simultaneously, mitochondria release membrane potential-indicating fluorophores like tetramethylrhodamine methylester. The MPT occurs in several forms of necrotic cell death, including oxidative stress, pH-dependent ischemia/reperfusion injury and Ca2+ ionophore toxicity. Cyclosporin A (CsA) and trifluoperazine block the MPT in these models and prevent cell killing, showing that the MPT is a causative factor in necrotic cell death. During oxidative injury induced by t-butylhydroperoxide, onset of the MPT is preceded by pyridine nucleotide oxidation, mitochondrial generation of reactive oxygen species, and an increase of mitochondrial free Ca2+, all changes that promote the MPT. During tissue ischemia, acidosis develops. Because of acidotic pH, anoxic cell death is substantially delayed. However, when pH is restored to normal after reperfusion (reoxygenation at pH 7.4), cell death occurs rapidly (pH paradox). This killing is caused by pH-dependent onset of the MPT, which is blocked by reperfusion at acidotic pH or with CsA. In isolated mitochondria, toxicants causing Reye’s syndrome, such as salicylate and valproate, induce the MPT. Similarly, salicylate induces a CsA-sensitive MPT and killing of cultured hepatocytes. These in vitro findings suggest that the MPT is the pathophysiological mechanism underlying Reye’s syndrome in vivo. Kroemer and coworkers proposed that the MPT is a critical event in the progression of apoptotic cell death. Using confocal microscopy, the MPT can be directly documented during tumor necrosis factor-α induced apoptosis in hepatocytes. CsA blocks this MPT and prevents apoptosis. The MPT does not occur uniformly during apoptosis. Initially, a small proportion of mitochondria undergo the MPT, which increases to nearly 100% over 1–3 h. A technique based on fluorescence resonance energy transfer can selectively reveal mitochondrial depolarization. After nutrient deprivation, a small fraction of mitochondria spontaneously depolarize and enter an acidic lysosomal compartment, suggesting that the MPT precedes the normal process of mitochondrial autophagy. A model is proposed in which onset of the MPT to increasing numbers of mitochondria within a cell leads progressively to autophagy, apoptosis and necrotic cell death

    Synthesis and Antibacterial Evaluation of a New Series of N-Alkyl-2-alkynyl/(E)-alkenyl-4-(1H)-quinolones

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    To gain further insight into the structural requirements of the aliphatic group at position 2 for their antimycobacterial activity, some N-alkyl-4-(1H)-quinolones bearing position 2 alkynyls with various chain length and triple bond positions were prepared and tested for in vitro antibacterial activity against rapidly-growing strains of mycobacteria, the vaccine strain Mycobacterium bovis BCG, and methicillin-resistant Staphylococcus aureus strains, EMRSA-15 and -16. The compounds were also evaluated for inhibition of ATP-dependent MurE ligase of Mycobacterium tuberculosis. The lowest MIC value of 0.5 mg/L (1.2–1.5 µM) was found against M. fortuitum and M. smegmatis. These compounds displayed no or only weak toxicity to the human lung fibroblast cell line MRC-5 at 100 µM concentration. The quinolone derivatives exhibited pronounced activity against the epidemic MRSA strains (EMRSA-15 and -16) with MIC values of 2–128 mg/L (5.3–364.7 µM), and M. bovis BCG with an MIC value of 25 mg/L (66.0–77.4 µM). In addition, the compounds inhibited the MurE ligase of M. tuberculosis with moderate to weak activity showing IC50 values of 200–774 µM. The increased selectivity towards mycobacterial bacilli with reference to MRC-5 cells observed for 2-alkynyl quinolones compared to their corresponding 2-alkenyl analogues serves to highlight the mycobacterial specific effect of the triple bond. Exploration of a terminal bromine atom at the side chain of N-alkyl-2-(E)-alkenyl-4-(1H)-quinolones showed improved antimycobacterial activity whereas a cyclopropyl residue at N-1 was suggested to be detrimental to antibacterial activity
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