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Mortality atlas     
Charlotte Gray 《CMAJ》1984,131(8):972-973
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Objective:To translate and validate into Greek, the SARC-F questionnaire, a screening tool for sarcopenia.Methods:Questionnaire was back-translated and culturally adapted into Greek according to guidelines proposed by the World Health Organization. A convenience sample of 197 Greek elderly people (71.6±7.8 years, 68.5% women) was recruited, 64 of which were classified as persons at risk of sarcopenia according to the SARC-F. Internal consistency, test-retest and inter-rater reliability were evaluated. Validity (sensitivity, specificity, predictive positive value and predictive negative value) was assessed against the definition from the European Working Group of Sarcopenia in Older People (EWGSOP2), which is considered gold standard. Receiver-operating characteristic analysis was also performed to calculate the area under the curve.Results:SARC-F demonstrated high internal consistency (Cronbach’s alpha of 0.93) and excellent inter-rater and test-retest reliability, with intraclass correlation coefficient (ICC) of 0.91 (95% CI 0.79-0.96), and 0.93 (95% CI 0.91-0.95), respectively. According to the definition of sarcopenia from the EWGSOP2, 53 (26.85) participants were identified as probable sarcopenic and 23 (11.6%) as sarcopenic. Sensitivity of the tool for sarcopenia was 34.4 and specificity was 93.2. Positive predictive values were 26.4 and negative predictive values were 66.6%.Conclusion:Τhe SARC-F was successfully adapted into Greek language. The Greek SARC-F revealed low sensitivity but high specificity with EWGSOP2 sarcopenia definitions, indicating that it can detect with precision the absence of sarcopenia.  相似文献   
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If two related plant species hybridize, their genomes may be combined and duplicated within a single nucleus, thereby forming an allotetraploid. How the emerging plant balances two co‐evolved genomes is still a matter of ongoing research. Here, we focus on satellite DNA (satDNA), the fastest turn‐over sequence class in eukaryotes, aiming to trace its emergence, amplification, and loss during plant speciation and allopolyploidization. As a model, we used Chenopodium quinoa Willd. (quinoa), an allopolyploid crop with 2n = 4x = 36 chromosomes. Quinoa originated by hybridization of an unknown female American Chenopodium diploid (AA genome) with an unknown male Old World diploid species (BB genome), dating back 3.3–6.3 million years. Applying short read clustering to quinoa (AABB), C. pallidicaule (AA), and C. suecicum (BB) whole genome shotgun sequences, we classified their repetitive fractions, and identified and characterized seven satDNA families, together with the 5S rDNA model repeat. We show unequal satDNA amplification (two families) and exclusive occurrence (four families) in the AA and BB diploids by read mapping as well as Southern, genomic, and fluorescent in situ hybridization. Whereas the satDNA distributions support C. suecicum as possible parental species, we were able to exclude C. pallidicaule as progenitor due to unique repeat profiles. Using quinoa long reads and scaffolds, we detected only limited evidence of intergenomic homogenization of satDNA after allopolyploidization, but were able to exclude dispersal of 5S rRNA genes between subgenomes. Our results exemplify the complex route of tandem repeat evolution through Chenopodium speciation and allopolyploidization, and may provide sequence targets for the identification of quinoa's progenitors.  相似文献   
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Biogeochemistry - Spectroscopy is a powerful means of increasing the availability of soil data necessary for understanding carbon cycling in a changing world. Here, we develop a calibration...  相似文献   
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Human DNA ligase I (LIG1) is the main replicative ligase and it also seals DNA breaks to complete DNA repair and recombination pathways. Immune compromised patients harbor hypomorphic LIG1 alleles encoding substitutions of conserved arginine residues, R771W and R641L, that compromise LIG1 activity through poorly defined mechanisms. To understand the molecular basis of LIG1 syndrome mutations, we determined high resolution X-ray structures and performed systematic biochemical characterization of LIG1 mutants using steady-state and pre-steady state kinetic approaches. Our results unveil a cooperative network of plastic DNA-LIG1 interactions that connect DNA substrate engagement with productive binding of Mg2+ cofactors for catalysis. LIG1 syndrome mutations destabilize this network, compromising Mg2+ binding affinity, decreasing ligation efficiency, and leading to elevated abortive ligation that may underlie the disease pathology. These findings provide novel insights into the fundamental mechanism by which DNA ligases engage with a nicked DNA substrate, and they suggest that disease pathology of LIG1 syndrome could be modulated by Mg2+ levels.  相似文献   
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