4,719 research outputs found
The SF-36: a simple, effective measure of mobility disability for epidemiological studies
No full textBackgroundMobility disability is a major problem in older people. Numerous scales exist for the measurement of disability but often these do not permit comparisons between study groups. The physical functioning (PF) domain of the established and widely used Short Form-36 (SF-36) questionnaire asks about limitations on ten mobility activities.ObjectivesTo describe prevalence of mobility disability in an elderly population, investigate the validity of the SF-36 PF score as a measure of mobility disability, and to establish age and sex specific norms for the PF score.MethodsWe explored relationships between the SF-36 PF score and objectively measured physical performance variables among 349 men and 280 women, 59-72 years of age, who participated in the Hertfordshire Cohort Study (HCS). Normative data were derived from the Health Survey for England (HSE) 1996.Results32% of men and 46% of women had at least some limitation in PF scale items. Poor SF-36 PF scores (lowest fifth of the gender-specific distribution) were related to: lower grip strength; longer timed-up-and-go, 3m walk, and chair rises test times in men and women; and lower quadriceps peak torque in women but not men. HSE normative data showed that median PF scores declined with increasing age in men and women.ConclusionOur results are consistent with the SF-36 PF score being a valid measure of mobility disability in epidemiological studies. This approach might be a first step towards enabling simple comparisons of prevalence of mobility disability between different studies of older people. The SF-36 PF score could usefully complement existing detailed schemes for classification of disability and it now requires validation against them
The telomerase-recruitment domain of the telomere binding protein Cdc13 is regulated by Mec1p/Tel1p-dependent phosphorylation
No full textProofreading activity of DNA polymerase Pol2 mediates 3’-end processing during nonhomologous end joining in yeast.
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SF Gospel: Blog contents, 2006-2015
No full textSF Gospel (2006-2015) was a blog exploring religious and theological themes in science fiction and popular culture by Gabriel Mckee, author of The Gospel According to Science Fiction. The primary PDF contains the textual content of the blog, along with most images that accompanied the original posts. The appendix PDF contains guest posts written by Mckee for other blogs and websites (including SF Signal, Holy Heroes, Nerve.com, and Religion Dispatches) during the course of SF Gospel's existence
Additional Files for Master Thesis "Framing Diets for Policy to Fight Climate Change"
No full textAdditional files for Master Thesis "Framing Diets for Policy to Fight Climate Change: Using video messages to measure the effect of goal framing on attitudes and intentions to reduce beef and dairy consumption to fight climate change"
Datasets
Intervention Framed Videos
Written within the M.Sc. Public Policy and Human Development at Maastricht University MGSoG/UNU-MERIT
Author: Sten Ritterfeld
Supervisor: Michelle González Amador
Submission date: July 12, 202
Rapid Cdc13 turnover and telomere length homeostasis are controlled by Cdk1-mediated phosphorylation of Cdc13.
No full textBudding yeast telomerase is mainly activated by Tel1/Mec1 (yeast ATM/ATR) on Cdc13 from late S to G2 phase of the cell cycle. Here, we demonstrated that the telomerase-recruitment domain of Cdc13 is also phosphorylated by Cdk1 at the same cell cycle stage as the Tel1/Mec1-dependent regulation. Phosphor-specific gel analysis demonstrated that Cdk1 phosphorylates residues 308 and 336 of Cdc13. The residue T308 of Cdc13 is critical for efficient Mec1-mediated S306 phosphorylation in vitro. Phenotypic analysis in vivo revealed that the mutations in the Cdc13 S/TP motifs phosphorylated by Cdk1 caused cell cycle delay and telomere shortening and these phenotypes could be partially restored by the replacement with a negative charge residue. In the absence of Ku or Tel1, Cdk1-mediated phosphorylation of Cdc13 showed no effect on telomere length maintenance. Moreover, this Cdk1-mediated phosphorylation was required to promote the regular turnover of Cdc13. Together these results demonstrate that Cdk1 phosphorylates the telomerase recruitment domain of Cdc13, thereby preserves optimal function and expression level of Cdc13 for precise telomere replication and cell cycle progression
Involvement of replicative polymerases, Tel1p, Mec1p, Cdc13p, and the Ku complex in telomere-telomere recombination.
No full textABSTRACT
Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of the reverse transcriptase telomerase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Genetic studies have led to the identification of DNA polymerases, cell cycle checkpoint proteins, and telomere binding proteins involved in the telomerase pathway. However, how these proteins affect telomere-telomere recombination has not been identified to date. Using an assay to trace the in vivo recombinational products throughout the course of survivor development, we show here that three major replicative polymerases, α, δ, and ε, play roles in telomere-telomere recombination and that each causes different effects and phenotypes when they as well as the telomerase are defective. Polymerase δ appears to be the main activity for telomere extension, since neither type I nor type II survivors arising via telomere-telomere recombination were seen in its absence. The frequency of type I versus type II is altered in the polymerase α and ε mutants relative to the wild type. Each prefers to develop a particular type of survivor. Moreover, type II recombination is mediated by the cell cycle checkpoint proteins Tel1 and Mec1, and telomere-telomere recombination is regulated by telomere binding protein Cdc13 and the Ku complex. Together, our results suggest that coordination between DNA replication machinery, DNA damage signaling, DNA recombination machinery, and the telomere protein-DNA complex allows telomere recombination to repair telomeric ends in the absence of telomerase.</jats:p
Systematic investigation of gastrointestinal diseases in China (SILC): validation of survey methodology
Full text linkBackground: Symptom-based surveys suggest that the prevalence of gastrointestinal diseases is lower in China than in Western countries. The aim of this study was to validate a methodology for the epidemiological investigation of gastrointestinal symptoms and endoscopic findings in China. Methods: A randomized, stratified, multi-stage sampling methodology was used to select 18 000 adults aged 18-80 years from Shanghai, Beijing, Xi'an, Wuhan and Guangzhou. Participants from Shanghai were invited to provide blood samples and undergo upper gastrointestinal endoscopy. All participants completed Chinese versions of the Reflux Disease Questionnaire (RDQ) and the modified Rome II questionnaire; 20% were also invited to complete the 36-item Short Form Health Survey (SF-36) and Epworth Sleepiness Scale (ESS). The psychometric properties of the questionnaires were evaluated statistically. Results: The study was completed by 16 091 individuals (response rate: 89.4%), with 3219 (89.4% of those invited) completing the SF-36 and ESS. All 3153 participants in Shanghai provided blood samples and 1030 (32.7%) underwent endoscopy. Cronbach's alpha coefficients were 0.89, 0.89, 0.80 and 0.91, respectively, for the RDQ, modified Rome II questionnaire, ESS and SF-36, supporting internal consistency. Factor analysis supported construct validity of all questionnaire dimensions except SF-36 psychosocial dimensions. Conclusion: This population-based study has great potential to characterize the relationship between gastrointestinal symptoms and endoscopic findings in China.Xiaoyan Yan, Rui Wang, Yanfang Zhao, Xiuqiang Ma, Jiqian Fang, Hong Yan, Xiaoping Kang, Ping Yin, Yuantao Hao, Qiang Li, John Dent, Joseph Sung, Duowu Zou, Saga Johansson, Katarina Halling, Wenbin Liu and Jia H
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