243 research outputs found

    Resistance training and youth

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    This is the publisher's version, also found at http://ehis.ebscohost.com/ehost/detail?vid=4&sid=34ab1967-2aea-457b-b261-e90e7b05e38c%40sessionmgr11&hid=2&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=s3h&AN=20752095The use of resistance training for children has increased in popularity and interest. It appears that children are capable of voluntary strength gains. Exercise prescription in younger populations is critical and requires certain program variables to be altered tTom adult perspectives. Individualization is vital, as the rate of physiological maturation has an impact on the adaptations that occur, The major difference in programs for children is the use of lighter loads (i.e., > 6 RM loads). It appears that longer duration programs (i.e., 10-20 wks) are better for observing training adaptations. This may be due to the fact that it takes more exercise to stimulate adaptational mechanisms related to strength performance beyond that of normal growth rates. The risk of injury appears low during participation in a resistance training program, and this risk is minimized with proper supervision and instruction. Furthermore, with the incidence of injury in youth sports, participation in a resistance training program may provide a protective advantage in one's preparation for sports participation

    Calibrating Emission Lines as Quasar Bolometers

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    Historically, emission lines have been considered a valuable tool for estimating the bolometric thermal luminosity of the accretion flow in AGN, LbolL_{bol}. We study the reliability of this method by comparing line strengths to the optical/UV continuum luminosity of SDSS DR7 radio quiet quasars with 0.4<z<0.80.4<z<0.8. We find formulae for LbolL_{bol} as a function of single line strengths for the broad components of Hβ\beta and Mg II, as well as the narrow lines of [O III] and [O II]. We determine the standard errors of the formulae that are fitted to the data. Our new estimators are shown to be more accurate than archival line strength estimations in the literature. It is demonstrated that the broad lines are superior estimators of the continuum luminosity (and LbolL_{bol}) with HβH\beta being the most reliable. The fidelity of the each of the estimators is determined in the context of the SDSS DR7 radio loud quasars as an illustrative application of our results. In general, individual researchers can use our results as a tool to help decide if a particular line strength provides an adequate estimate of LbolL_{bol} for their purposes. Finally, it is shown that considering all four line strength, simultaneously, can yield information on both LbolL_{bol} and the radio jet power.Comment: To appear in MNRAS Letter

    Ethosuximide ameliorates neurodegenerative disease phenotypes by modulating DAF-16/FOXO target gene expression

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    Background Many neurodegenerative diseases are associated with protein misfolding/aggregation. Treatments mitigating the effects of such common pathological processes, rather than disease-specific symptoms, therefore have general therapeutic potential. Results Here we report that the anti-epileptic drug ethosuximide rescues the short lifespan and chemosensory defects exhibited by C. elegans null mutants of dnj-14, the worm orthologue of the DNAJC5 gene mutated in autosomal-dominant adult-onset neuronal ceroid lipofuscinosis. It also ameliorates the locomotion impairment and short lifespan of worms expressing a human Tau mutant that causes frontotemporal dementia. Transcriptomic analysis revealed a highly significant up-regulation of DAF-16/FOXO target genes in response to ethosuximide; and indeed RNAi knockdown of daf-16 abolished the therapeutic effect of ethosuximide in the worm dnj-14 model. Importantly, ethosuximide also increased the expression of classical FOXO target genes and reduced protein aggregation in mammalian neuronal cells. Conclusions We have revealed a conserved neuroprotective mechanism of action of ethosuximide from worms to mammalian neurons. Future experiments in mouse neurodegeneration models will be important to confirm the repurposing potential of this well-established anti-epileptic drug for treatment of human neurodegenerative diseases

    Pathological phosphorylation of tau and TDP-43 by TTBK1 and TTBK2 drives neurodegeneration

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    BACKGROUND: Progressive neuron loss in the frontal and temporal lobes of the cerebral cortex typifies frontotemporal lobar degeneration (FTLD). FTLD sub types are classified on the basis of neuronal aggregated protein deposits, typically containing either aberrantly phosphorylated TDP-43 or tau. Our recent work demonstrated that tau tubulin kinases 1 and 2 (TTBK1/2) robustly phosphorylate TDP-43 and co-localize with phosphorylated TDP-43 in human postmortem neurons from FTLD patients. Both TTBK1 and TTBK2 were initially identified as tau kinases and TTBK1 has been shown to phosphorylate tau epitopes commonly observed in Alzheimer's disease and other tauopathies. METHODS: To further elucidate how TTBK1/2 activity contributes to both TDP-43 and tau phosphorylation in the context of the neurodegeneration seen in FTLD, we examined the consequences of elevated human TTBK1/2 kinase expression in transgenic animal models of disease. RESULTS: We show that C. elegans co-expressing tau/TTBK1 tau/TTBK2, or TDP-43/TTBK1 transgenes in combination exhibit synergistic exacerbation of behavioral abnormalities and increased pathological protein phosphorylation. We also show that C. elegans co-expressing tau/TTBK1 or tau/TTBK2 transgenes in combination exhibit aberrant neuronal architecture and neuron loss. Surprisingly, the TTBK2/TDP-43 transgenic combination showed no exacerbation of TDP-43 proteinopathy related phenotypes. Additionally, we observed elevated TTBK1/2 protein expression in cortical and hippocampal neurons of FTLD-tau and FTLD-TDP cases relative to normal controls. CONCLUSIONS: Our findings suggest a possible etiology for the two most common FTLD subtypes through a kinase activation driven mechanism of neurodegeneration

    Portrayal of Alcohol Brands Popular Among Underage Youth on YouTube: A Content Analysis

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    Objective. We characterized leading YouTube videos featuring alcohol brand references and examined video characteristics associated with each brand and video category. Method. We systematically captured the 137 most relevant and popular videos on YouTube portraying alcohol brands that are popular among underage youth. We employed an iterative process to codebook development. We coded variables within domains of video type, character socio-demographics, production quality, and negative and positive associations with alcohol use. All variables were double coded, and Cohen’s κ>0.80 for all variables except age, which was eliminated. Results. There were 96,860,936 combined views for all videos. The most common video type was “traditional advertisements,” which comprised 40% of videos. Of the videos, 20% were “guides” and 10% focused on chugging a bottle of hard liquor. While 95% of videos featured males, 40% featured females. Alcohol intoxication was present in 19% of videos. Aggression, addiction, and injuries were uncommonly identified (2%, 3%, and 4%, respectively), but 47% of videos contained humor. Traditional advertisements represented the majority of videos related to Bud Light (83%) but only 18% of Grey Goose and 8% of Hennessy videos. Intoxication was most present in chugging demonstrations (77%), while addiction was only portrayed in music videos (22%). Videos containing humor ranged from 11% for music-related videos to 77% for traditional advertisements. Conclusions. YouTube videos depicting the alcohol brands favored by underage youth are heavily viewed, and the majority are traditional or narrative advertisements. Understanding characteristics associated with different brands and video categories may aid in intervention development

    The tau tubulin kinases TTBK1/2 promote accumulation of pathological TDP-43

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    Pathological aggregates of phosphorylated TDP-43 characterize amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD-TDP), two devastating groups of neurodegenerative disease. Kinase hyperactivity may be a consistent feature of ALS and FTLD-TDP, as phosphorylated TDP-43 is not observed in the absence of neurodegeneration. By examining changes in TDP-43 phosphorylation state, we have identified kinases controlling TDP-43 phosphorylation in a C. elegans model of ALS. In this kinome-wide survey, we identified homologs of the tau tubulin kinases 1 and 2 (TTBK1 and TTBK2), which were also identified in a prior screen for kinase modifiers of TDP-43 behavioral phenotypes. Using refined methodology, we demonstrate TTBK1 and TTBK2 directly phosphorylate TDP-43 in vitro and promote TDP-43 phosphorylation in mammalian cultured cells. TTBK1/2 overexpression drives phosphorylation and relocalization of TDP-43 from the nucleus to cytoplasmic inclusions reminiscent of neuropathologic changes in disease states. Furthermore, protein levels of TTBK1 and TTBK2 are increased in frontal cortex of FTLD-TDP patients, and TTBK1 and TTBK2 co-localize with TDP-43 inclusions in ALS spinal cord. These kinases may represent attractive targets for therapeutic intervention for TDP-43 proteinopathies such as ALS and FTLD-TDP
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