59 research outputs found

    Enhancement of Heat-Cured Cement Paste with Tannic Acid

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    The Improvement of Cement-Based Materials\u27 Performance by Natural Organic Compounds Can Greatly Promote the Green and Sustainable Development of the Construction Industry. However, Such Compounds Are Not Widely Used Yet Because of their Retarding Effect on Cement. in This Study, the Retardation Effect of Tannic Acid (TA, a Well-Known Retarding Compound) is overcome and the Enhancing Effect is Achieved by Adding Less Than 0.1% Content and Curing Samples in Thermal Regime. Then the Mechanism of TA Enhancing Heat-Cured Cement Pastes is Studied Systematically. Mechanical Properties Results Suggest that Addition of 0.025% TA Can Reduce the Compressive and Flexural Strengths of Cement Pastes by Up to 3.4% and 17.1% under Normal Curing Regime at 3 Days, But Enhance These Two Strengths by More Than 11.4% and 34.6% after Thermal Curing, Respectively. XRD Patterns and TGA Analysis Indicate that, under Thermal Curing Regime, 0.025% TA Can Improve the Hydration Degree of Cement Where the Bound Water Content is Increased by 21.4%. SEM Observations and MIP Results Show that TA Can Compact the Microstructure and the Porosity is Decreased by More Than 7.0%. Furthermore, FTIR Spectrums Prove that TA Can Bond with Hydration Products. Molecular Dynamics Simulation Demonstrates that TA Cross-Links with Calcium Silicate Hydrates (C–S–H) through Ionic and Hydrogen Bonds, Which Could Increase the Tensile Strength by 12.5% and the Ultimate Strain by 100%

    Wavelet Power and Shannon Entropy Applied to Acoustic Emission Signals for Corrosion Detection and Evaluation of Reinforced Concrete

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    Acoustic emission (AE) signals detected from corrosion test on a steel reinforced concrete beam subjected to the coupling effects of corrosive wet-dry cycles and static load are analyzed by power spectral density, wavelet transform, and Shannon entropy. The degradation process of the corroded reinforced concrete beam can be divided into four stages on the basis of the accumulated event number (AEN). Due to the difference of material properties, steel reinforcement and concrete matrix have distinguished AE features. The time-frequency characteristics of AE signals can reflect the microstructural degradation mechanism of steel corrosion and concrete cracking. The corrosion evaluation entails investigating the evolution of the wavelet power mathematically by Shannon entropy. The frequency-entropy clearly exhibits the relative power distribution of AE signal in a certain frequency region. With the accumulation of steel corrosion and concrete deterioration, the increment of the overall entropy integration is considerably apparent. The variation of frequency-entropy curve reveals the corrosion revolution of the reinforced concrete members under static load, which is represented by a transforming from corrosion-induced micro cracking to load-induced localized cracking

    Enhancement of Cement Paste with Carboxylated Carbon Nanotubes and Poly(Vinyl Alcohol)

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    Cement has been a major consumable material for construction in the world since its invention, but its low flexural strength is the main defect affecting the service life of structures. To adapt cement-based materials to a more stringent environment, carboxylated carbon nanotubes (CNTs-COOH) and poly(vinyl alcohol) (PVA) are proposed to enhance the mechanical properties of cement paste. This study systematically verifies the synergistic effect of CNTs-COOH/PVA on the performance of cement paste. First, UV-Vis spectroscopy and FTIR spectroscopy prove that CNTs-COOH can provide attachment sites for PVA and PVA can improve the dispersion and stability of CNTs-COOH in water, which demonstrates the feasibility of synergistically enhancing cement paste. When a 0.015% CNTs-COOH suspension with 0.1% PVA is added, the flexural strength of the cement paste increases by 73, 32, and 42% compared with control specimens at curing ages of 3, 7, and 28 days, respectively. The strength enhancement mechanism is revealed from the aspects of cement matrix enhancement and interface enhancement. Thermogravimetric (TG) analysis and mercury intrusion porosimetry (MIP) prove that CNTs-COOH can enhance the hydration degree of the cement matrix and fill the pores introduced by PVA. Based on the fact that PVA can improve the dispersibility and the nucleation site effect of CNTs-COOH in cement paste, molecular dynamics simulation confirms that PVA can bridge CNTs-COOH and C-S-H to enhance the interfacial bonding by 64.1%

    Translational control of cardiac fibrosis

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    Background Fibrosis is a common pathology in many cardiac disorders and is driven by the activation of resident fibroblasts. The global post-transcriptional mechanisms underlying fibroblast-to-myofibroblast conversion in the heart have not been explored. Methods Genome-wide changes of RNA transcription and translation during human cardiac fibroblast activation were monitored with RNA sequencing and ribosome profiling. We then used miRNA-and RNA-binding protein-based analyses to identify translational regulators of fibrogenic genes. To reveal post-transcriptional mechanisms in the human fibrotic heart, we then integrated our findings with cardiac ribosome occupancy levels of 30 dilated cardiomyopathy patients. Results We generated nucleotide-resolution translatome data during the TGFβ1-driven cellular transition of human cardiac fibroblasts to myofibroblasts. This identified dynamic changes of RNA transcription and translation at several time points during the fibrotic response, revealing transient and early-responder genes. Remarkably, about one-third of all changes in gene expression in activated fibroblasts are subject to translational regulation and dynamic variation in ribosome occupancy affects protein abundance independent of RNA levels. Targets of RNA-binding proteins were strongly enriched in post-transcriptionally regulated genes, suggesting genes such as MBNL2 can act as translational activators or repressors. Ribosome occupancy in the hearts of patients with dilated cardiomyopathy suggested an extensive post-transcriptional regulatory network underlying cardiac fibrosis. Key network hubs include RNA-binding proteins such as PUM2 and QKI that work in concert to regulate the translation of target transcripts in human diseased hearts. Conclusions We reveal widespread translational effects of TGFβ1 and define novel post-transcriptional events that control the fibroblast-to-myofibroblast transition. Regulatory networks that affect ribosome occupancy in fibroblasts are paralleled in human heart disease. Our findings show the central importance of translational control in fibrosis and highlight novel pathogenic mechanisms in heart failure

    Genetic Drivers of Heterogeneity in Type 2 Diabetes Pathophysiology

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    Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P \u3c 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care

    Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

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    Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P &lt; 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p

    RESPIRABLE SIRNA TARGETING AT THE NF-KB PATHWAY PROTECTS AGAINST INFLAMMATORY LUNG DISEASES

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    Ph.DDOCTOR OF PHILOSOPH

    Hepatocyte Specific gp130 Signalling Underlies APAP Induced Liver Injury

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    N-acetyl-p-aminophenol (APAP)-induced liver damage is associated with upregulation of Interleukin-11 (IL11), which is thought to stimulate IL6ST (gp130)-mediated STAT3 activity in hepatocytes, as a compensatory response. However, recent studies have found IL11/IL11RA/gp130 signaling to be hepatotoxic. To investigate further the role of IL11 and gp130 in APAP liver injury, we generated two new mouse strains with conditional knockout (CKO) of either Il11 (CKOIl11) or gp130 (CKOgp130) in adult hepatocytes. Following APAP, as compared to controls, CKOgp130 mice had lesser liver damage with lower serum Alanine Transaminase (ALT) and Aspartate Aminotransferase (AST), greatly reduced serum IL11 levels (90% lower), and lesser centrilobular necrosis. Livers from APAP-injured CKOgp130 mice had lesser ERK, JNK, NOX4 activation and increased markers of regeneration (PCNA, Cyclin D1, Ki67). Experiments were repeated in CKOIl11 mice that, as compared to wild-type mice, had lower APAP-induced ALT/AST, reduced centrilobular necrosis and undetectable IL11 in serum. As seen with CKOgp130 mice, APAP-treated CKOIl11 mice had lesser ERK/JNK/NOX4 activation and greater features of regeneration. Both CKOgp130 and CKOIl11 mice had normal APAP metabolism. After APAP, CKOgp130 and CKOIl11 mice had reduced Il6, Ccl2, Ccl5, Il1&beta;, and Tnf&alpha; expression. These studies exclude IL11 upregulation as compensatory and establish autocrine, self-amplifying, gp130-dependent IL11 secretion from damaged hepatocytes as toxic and anti-regenerative

    Quantitative Evaluation of Steel Corrosion Induced Deterioration in Rubber Concrete by Integrating Ultrasonic Testing, Machine Learning and Mesoscale Simulation

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    Chloride-induced steel corrosion seriously affects the durability of reinforced concrete structures. Rubber concrete, an environmentally friendly construction material in which waste rubber is recycled as a concrete component, has demonstrated superior resistance to chloride-induced steel corrosion and the subsequent concrete deterioration. However, quantitative evaluation of the degree of deterioration in rubber concrete based on nondestructive detection is challenging due to the complexity of the material. In this paper, reinforced concrete specimens with rubber contents of 0, 10% and 20% are subjected to the electrochemically accelerated corrosion experiments and monitored by ultrasonic testing. Six machine learning models are trained by the data derived from the ultrasonic testing to predict the corrosion degree based on ultrasonic traits. The results show that the machine learning models except for the linear model can accurately and robustly predict the corrosion degree under the interference of outlier amplitude and size of training set. Furthermore, the corrosion-induced deterioration process is computed by mesoscale simulation based on the corrosion degree, so that the damages of specimens with different rubber contents are quantitatively evaluated. The experimental and computational studies prove that the addition of rubber into concrete effectively retards the corrosion of steel and the deterioration of concrete

    Corrosion monitoring of reinforced concrete beam using embedded cementbased piezoelectric sensor

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    The corrosion of reinforcement is a well-recognised problem in the maintenance of concrete structures that can lead to reduction of the cross-section of the rebar, thus weakening the load-carrying capacity of the structure. Under ordinary design conditions, cracks are allowed to appear in concrete beams. However, the existence of cracks can speed up the corrosion rate of reinforcement significantly. In this study, the corrosion activities of reinforcement in concrete beams with or without cracks under accelerated corrosion conditions were monitored using embedded cement-based piezoelectric composite sensors and the acoustic emission (AE) technique. The AEs generated by the initiation of localised corrosion and subsequent concrete cracks were successfully detected and recorded by a homeprogrammed DEcLIN monitoring system. Based on frequency domain identification, useful information was extracted to explain the process of deterioration of concrete structures. It was found that cement-based piezoelectric sensors show a good capability in AE detection and the beam with cracks corroded much earlier than the case without cracking, consequently resulting in early deterioration
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