132 research outputs found

    The Effects of Salt on Rheological Properties of Asphalt after Long-Term Aging

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    Limited studies in recent years have shown that asphalt pavement subject to seawater in coastal regions or deicing salt in cold regions may be seriously damaged after being soaked in saline water for a long time. However, there is limited research into the influence of salt on rheological properties of asphalt after long-term aging. In this study, rheological properties of unmodified and polymer-modified asphalt after long-term aging were tested after being soaked in different concentrations of salt (0.3%~5%) for different durations (1 day~30 days). Orthogonal array based on the Taguchi method was used for experimental design. The frequency sweep tests were performed on the specimens of aged asphalt after being soaked for complex modulus and phase angle master curves and ultimate fatigue temperature. BBR tests were performed for stiffness. The test results indicate that saline water appears to reduce low temperature properties and fatigue resistance properties and improved high temperature properties of aged asphalt, and it also affects the sensitivity of complex modulus and phase angles at low frequencies

    Analysis of Flavor Characteristics and Characteristic Components of White Tea Made from Oolong Tea Cultivars

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    In order to investigate the differences in flavor quality between white tea made from Oolong tea cultivars and traditional white tea, white teas made from eight Oolong tea cultivars such as Zimeigui and Fuding Dahao white tea as a control were analyzed by sensory evaluation, biochemical assays and multivariate statistical analysis. The results showed that the appearance and infusion color of Oolong white tea were darker, while the taste and aroma were better than those of traditional white tea. The biochemical analysis revealed that the differences in conductivity, pH, and the contents of soluble sugars, free amino acids, gallocatechin gallate (GCG) and epigallocatechin gallate (EGCG) were important factors causing the differences in taste between traditional white tea and white tea made from Oolong tea cultivars. Volatile composition analysis showed that trans-2-nonenal, cis-3-nonen-1-ol, methyl palmitate, linalool, methyl linoleate, cedrol, geranyl formate, phenethyl alcohol, nerolidol, methyl salicylate, dibutyl phthalate and phytone were the key differential aroma components contributing to the difference in aroma between Oolong and traditional white tea. Findings from this study will provide a theoretical reference for flavor diversification of white tea

    Transposable element-initiated enhancer-like elements generate the subgenome-biased spike specificity of polyploid wheat

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    Transposable elements (TEs) comprise ~85% of the common wheat genome, which are highly diverse among subgenomes, possibly contribute to polyploid plasticity, but the causality is only assumed. Here, by integrating data from gene expression cap analysis and epigenome profiling via hidden Markov model in common wheat, we detect a large proportion of enhancer-like elements (ELEs) derived from TEs producing nascent noncoding transcripts, namely ELE-RNAs, which are well indicative of the regulatory activity of ELEs. Quantifying ELE-RNA transcriptome across typical developmental stages reveals that TE-initiated ELE-RNAs are mainly from RLG_famc7.3 specifically expanded in subgenome A. Acquisition of spike-specific transcription factor binding likely confers spike-specific expression of RLG_famc7.3-initiated ELE-RNAs. Knockdown of RLG_famc7.3-initiated ELE-RNAs resulted in global downregulation of spike-specific genes and abnormal spike development. These findings link TE expansion to regulatory specificity and polyploid developmental plasticity, highlighting the functional impact of TE-driven regulatory innovation on polyploid evolution

    Substantial transition to clean household energy mix in rural China

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    The household energy mix has significant impacts on human health and climate, as it contributes greatly to many health- and climate-relevant air pollutants. Compared to the well-established urban energy statistical system, the rural household energy statistical system is incomplete and is often associated with high biases. Via a nationwide investigation, this study revealed high contributions to energy supply from coal and biomass fuels in the rural household energy sector, while electricity comprised ∌20%. Stacking (the use of multiple sources of energy) is significant, and the average number of energy types was 2.8 per household. Compared to 2012, the consumption of biomass and coals in 2017 decreased by 45% and 12%, respectively, while the gas consumption amount increased by 204%. Increased gas and decreased coal consumptions were mainly in cooking, while decreased biomass was in both cooking (41%) and heating (59%). The time-sharing fraction of electricity and gases (E&G) for daily cooking grew, reaching 69% in 2017, but for space heating, traditional solid fuels were still dominant, with the national average shared fraction of E&G being only 20%. The non-uniform spatial distribution and the non-linear increase in the fraction of E&G indicated challenges to achieving universal access to modern cooking energy by 2030, particularly in less-developed rural and mountainous areas. In some non-typical heating zones, the increased share of E&G for heating was significant and largely driven by income growth, but in typical heating zones, the time-sharing fraction was <5% and was not significantly increased, except in areas with policy intervention. The intervention policy not only led to dramatic increases in the clean energy fraction for heating but also accelerated the clean cooking transition. Higher income, higher education, younger age, less energy/stove stacking and smaller family size positively impacted the clean energy transition

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∌99% of the euchromatic genome and is accurate to an error rate of ∌1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    La trajectoire non télomérique de l'évolution de TRF2 chez le poisson zÚbre révÚle le rÎle que joue cette protéine au cours du neurodéveloppement

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    The shelterin protein complex is a key player of telomere protection, a process inextricably linked to ageing. Accordingly, decrease in shelterin expression is associated with increasing age in many organisms. Here we demonstrate that the zebrafish ortholog of the mammalian shelterin subunit TRF2 (zfTRF2 encoded by the TERFA gene) exhibits a higher expression in neural system decreasing during aging. Further investigation shows that zebrafish TRF2 is required to prevent ATM-dependent DNA damage signaling, but not specifically at the telomeres. Complete TERFA ablation induced severe embryonic neurodevelopmental failure and death, whereas TERFA haploinsufficiency led to premature aging in adult fishes. Remarkably, ATM inhibition completely prevented DNA damage signaling in terfa-compromised embryos but led to only partial recovery from embryonic neurodevelopmental failure, suggesting that zfTRF2 controls processes other than genome stability. Indeed, overexpressing genes that were downregulated in terfa-compromised embryos had an epistatic effect with ATM inhibition, resulting in a better recovery from neurodevelopmental failure. Furthermore, glial cell-specific restoration of zfTRF2 expression was sufficient to rescue the embryonic neurodevelopment phenotype, unveiling a key neurodevelopmental role of zfTRF2 in glial cells. Our results suggest that the key shelterin subunit TRF2 evolved in zebrafish as a general genome caretaker that is required for proper neurodevelopment by both preventing DNA damage signaling and regulating gene expression. I propose a model of telomere evolution based on the redeployment of general factors involved in genome maintenance, coupling telomere status to development and aging.Mon projet de doctorat est de comprendre la fonction de la protĂ©ine TERF2 sous-unitĂ© du complexe shelterin dans le poisson zĂšbre. Je prĂ©sente mon travail en deux parties. J’ai d’abord utilisĂ© deux modĂšles animaux diffĂ©rents et mesurĂ© le niveau d’ARNm et le niveau de protĂ©ine des gĂšnes de shelterin dans divers tissues pendant le dĂ©veloppement de la souris et pendant la vie adulte chez le poisson zĂšbre. J’ai rĂ©vĂ©lĂ© que les sous-unitĂ©s de shelterin prĂ©sentent des expressions spatiales et temporelles distinctes qui ne sont pas corrĂ©lĂ©es avec le statut prolifĂ©ratif des organes examinĂ©s. Par exemple, le gĂšne terfa (gĂšne codant pour TRF2 chez les poissons zĂšbres) est beaucoup plus Ă©levĂ© dans le cerveau que dans d’autres tissus au cours du dĂ©veloppement et chez l’ adulte et diminue fortement avec l’ñge. Ceci suggĂšre une fonction particuliĂšre de TRF2 dans le cerveau pendant le dĂ©veloppement et le vieillissement, indĂ©pendamment de sa fonction de protection des telomere. Ainsi, dans la deuxiĂšme partie, je me suis concentrĂ© sur la façon dont TRF2 fonctionne pendant le dĂ©veloppement du poisson zĂšbre, en particulier pour comprendre la fonction extra-tĂ©lomĂ©rique de TRF2 dans le dĂ©veloppement neuronal. J’ai pu montrĂ© que l’ortholog chez le poisson zĂšbre de TRF2 (zfTRF2 codĂ© par le gĂšne TERFA) joue un rĂŽle gĂ©nĂ©ral dans la protection du gĂ©nome sans spĂ©cificitĂ© apparente pour la protection des tĂ©lomĂšres. Afin d’explorer le rĂŽle de zfTRF2 in vivo, j’ai gĂ©nĂ©rĂ© un modĂšle de poisson zĂšbre invalidĂ©s pour terfa. J’ai dĂ©montrĂ© que zfTRF2 est nĂ©cessaire pour empĂȘcher la signalisation des dommages de l’ADN mais pas spĂ©cifiquement aux tĂ©lomĂšres. Une ablation complĂšte de terfa induit une insuffisance et une mort embryonnaire avec des dĂ©fauts majeurs du systĂšme nerveux tandis que son haploinsuffisance mĂšne Ă  un phĂ©notype de vieillissement prĂ©maturĂ© chez l’adulte. L’inhibition des points de contrĂŽle de la rĂ©ponse Ă  l’ADN endommagĂ© chez les embryons compromis pour terfa ne permet pas ’une rĂ©cupĂ©ration complkĂšte des dĂ©fauts neurodĂ©veloppementaux, ce qui suggĂšre que zfTRF2 contrĂŽle d’autres processus que la stabilitĂ© du gĂ©nome. En effet, restaurer l’expression de gĂšnes rĂ©gulĂ©s par zfTRF2 agit de maniĂšre epistatique avec l’inhibition de la rĂ©ponse au dommage Ă  l’ADN pour amĂ©liorer les problĂšmes neurodĂ©veloppementaux des poissons compromis pour terfa. Une restauration spĂ©cifique de l’expression zfTRF2 dans les cellules gliales est suffisante pour amĂ©liorer le phĂ©notype embryonnaire de neurodĂ©veloppement, dĂ©voilant un rĂŽle clĂ© de zfTRF2 dans les cellules gliales pendant le neurodĂ©veloppement. Ainsi, ces rĂ©sultats rĂ©vĂšlent qu’une sous-unitĂ© de shelterin a Ă©voluĂ© dans le poisson zĂšbre en tant que gardien gĂ©nĂ©ral de gĂ©nome nĂ©cessaire pour un neurodĂ©veloppement appropriĂ© en empĂȘchant la signalisation de dommages d’ADN et en rĂ©gulant l’expression spĂ©cifique de gĂšnes cibles.Ces travaux posent la question des mĂ©canismes de protection des tĂ©lomĂšres chez le poisson zĂšbre et de connaitre le dĂ©tail des mĂ©canismes molĂ©culaires qui rĂ©gissent le rĂŽle spĂ©cifique de TRF2 dans les cellules gliales pour rĂ©guler le dĂ©veloppement neuronal

    The non-telomeric evolutionary trajectory of TRF2 in zebrafish reveals its essential role in neurodevelopment and aging

    No full text
    Mon projet de doctorat est de comprendre la fonction de la protĂ©ine TERF2 sous-unitĂ© du complexe shelterin dans le poisson zĂšbre. Je prĂ©sente mon travail en deux parties. J’ai d’abord utilisĂ© deux modĂšles animaux diffĂ©rents et mesurĂ© le niveau d’ARNm et le niveau de protĂ©ine des gĂšnes de shelterin dans divers tissues pendant le dĂ©veloppement de la souris et pendant la vie adulte chez le poisson zĂšbre. J’ai rĂ©vĂ©lĂ© que les sous-unitĂ©s de shelterin prĂ©sentent des expressions spatiales et temporelles distinctes qui ne sont pas corrĂ©lĂ©es avec le statut prolifĂ©ratif des organes examinĂ©s. Par exemple, le gĂšne terfa (gĂšne codant pour TRF2 chez les poissons zĂšbres) est beaucoup plus Ă©levĂ© dans le cerveau que dans d’autres tissus au cours du dĂ©veloppement et chez l’ adulte et diminue fortement avec l’ñge. Ceci suggĂšre une fonction particuliĂšre de TRF2 dans le cerveau pendant le dĂ©veloppement et le vieillissement, indĂ©pendamment de sa fonction de protection des telomere. Ainsi, dans la deuxiĂšme partie, je me suis concentrĂ© sur la façon dont TRF2 fonctionne pendant le dĂ©veloppement du poisson zĂšbre, en particulier pour comprendre la fonction extra-tĂ©lomĂ©rique de TRF2 dans le dĂ©veloppement neuronal. J’ai pu montrĂ© que l’ortholog chez le poisson zĂšbre de TRF2 (zfTRF2 codĂ© par le gĂšne TERFA) joue un rĂŽle gĂ©nĂ©ral dans la protection du gĂ©nome sans spĂ©cificitĂ© apparente pour la protection des tĂ©lomĂšres. Afin d’explorer le rĂŽle de zfTRF2 in vivo, j’ai gĂ©nĂ©rĂ© un modĂšle de poisson zĂšbre invalidĂ©s pour terfa. J’ai dĂ©montrĂ© que zfTRF2 est nĂ©cessaire pour empĂȘcher la signalisation des dommages de l’ADN mais pas spĂ©cifiquement aux tĂ©lomĂšres. Une ablation complĂšte de terfa induit une insuffisance et une mort embryonnaire avec des dĂ©fauts majeurs du systĂšme nerveux tandis que son haploinsuffisance mĂšne Ă  un phĂ©notype de vieillissement prĂ©maturĂ© chez l’adulte. L’inhibition des points de contrĂŽle de la rĂ©ponse Ă  l’ADN endommagĂ© chez les embryons compromis pour terfa ne permet pas ’une rĂ©cupĂ©ration complkĂšte des dĂ©fauts neurodĂ©veloppementaux, ce qui suggĂšre que zfTRF2 contrĂŽle d’autres processus que la stabilitĂ© du gĂ©nome. En effet, restaurer l’expression de gĂšnes rĂ©gulĂ©s par zfTRF2 agit de maniĂšre epistatique avec l’inhibition de la rĂ©ponse au dommage Ă  l’ADN pour amĂ©liorer les problĂšmes neurodĂ©veloppementaux des poissons compromis pour terfa. Une restauration spĂ©cifique de l’expression zfTRF2 dans les cellules gliales est suffisante pour amĂ©liorer le phĂ©notype embryonnaire de neurodĂ©veloppement, dĂ©voilant un rĂŽle clĂ© de zfTRF2 dans les cellules gliales pendant le neurodĂ©veloppement. Ainsi, ces rĂ©sultats rĂ©vĂšlent qu’une sous-unitĂ© de shelterin a Ă©voluĂ© dans le poisson zĂšbre en tant que gardien gĂ©nĂ©ral de gĂ©nome nĂ©cessaire pour un neurodĂ©veloppement appropriĂ© en empĂȘchant la signalisation de dommages d’ADN et en rĂ©gulant l’expression spĂ©cifique de gĂšnes cibles.Ces travaux posent la question des mĂ©canismes de protection des tĂ©lomĂšres chez le poisson zĂšbre et de connaitre le dĂ©tail des mĂ©canismes molĂ©culaires qui rĂ©gissent le rĂŽle spĂ©cifique de TRF2 dans les cellules gliales pour rĂ©guler le dĂ©veloppement neuronal.The shelterin protein complex is a key player of telomere protection, a process inextricably linked to ageing. Accordingly, decrease in shelterin expression is associated with increasing age in many organisms. Here we demonstrate that the zebrafish ortholog of the mammalian shelterin subunit TRF2 (zfTRF2 encoded by the TERFA gene) exhibits a higher expression in neural system decreasing during aging. Further investigation shows that zebrafish TRF2 is required to prevent ATM-dependent DNA damage signaling, but not specifically at the telomeres. Complete TERFA ablation induced severe embryonic neurodevelopmental failure and death, whereas TERFA haploinsufficiency led to premature aging in adult fishes. Remarkably, ATM inhibition completely prevented DNA damage signaling in terfa-compromised embryos but led to only partial recovery from embryonic neurodevelopmental failure, suggesting that zfTRF2 controls processes other than genome stability. Indeed, overexpressing genes that were downregulated in terfa-compromised embryos had an epistatic effect with ATM inhibition, resulting in a better recovery from neurodevelopmental failure. Furthermore, glial cell-specific restoration of zfTRF2 expression was sufficient to rescue the embryonic neurodevelopment phenotype, unveiling a key neurodevelopmental role of zfTRF2 in glial cells. Our results suggest that the key shelterin subunit TRF2 evolved in zebrafish as a general genome caretaker that is required for proper neurodevelopment by both preventing DNA damage signaling and regulating gene expression. I propose a model of telomere evolution based on the redeployment of general factors involved in genome maintenance, coupling telomere status to development and aging
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