7 research outputs found

    Direct Coating Adherent Diamond Films on Fe-Based Alloy Substrate: The Roles of Al, Cr in Enhancing Interfacial Adhesion and Promoting Diamond Growth

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    Direct CVD deposition of dense, continuous, and adherent diamond films on conventional Fe-based alloys has long been considered impossible. The current study demonstrates that such a deposition can be realized on Al, Cr-modified Fe-based alloy substrate (FeAl or FeCrAl). To clarify the fundamental mechanism of Al, Cr in promoting diamond growth and enhancing interfacial adhesion, fine structure and chemical analysis around the diamond film–substrate interface have been comprehensively characterized by transmission electron microscopy. An intermediate graphite layer forms on those Al-free substrates such as pure Fe and FeCr, which significantly deteriorates the interfacial adhesion of diamond. In contrast, such a graphite layer is absent on the FeAl and FeCrAl substrates, whereas a very thin Al-rich amorphous oxide sublayer is always identified between the diamond film and substrate interface. These comparative results indicate that the Al-rich interfacial oxide layer acts as an effective barrier to prevent the formation of graphite phase and consequently enhance diamond growth and adhesion. The adhesion of diamond film formed on FeCrAl is especially superior to that formed on FeAl substrate. This can be further attributed to a synergetic effect including the reduced fraction of Al and the decreased substrate thermal-expansion coefficient on FeCrAl in comparison with FeAl, and a mechanical interlocking effect due to the formation of interfacial chromium carbides. Accordingly, a mechanism model is proposed to account for the different interfacial adhesion of diamond grown on the various Fe-based substrates

    Injection of CO<sub>2</sub>‑Saturated Water through a Siliceous Sandstone Plug from the Hontomin Test Site (Spain): Experiment and Modeling

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    Massive chemical reactions are not expected when injecting CO<sub>2</sub> in siliceous sandstone reservoirs, but their performance can be challenged by small-scale reactions and other processes affecting their transport properties. We have conducted a core flooding test with a quartzarenite plug of Lower Cretaceous age representative of the secondary reservoir of the Hontomín test site. The sample, confined at high pressure, was successively injected with DIW and CO<sub>2</sub>-saturated DIW for 49 days while monitoring geophysical, chemical, and hydrodynamic parameters. The plug experienced little change, without evidence of secondary carbonation. However, permeability increased by a factor of 4 (0.022–0.085 mD), and the <i>V</i><sub>P</sub>/<i>V</i><sub>S</sub> ratio, whose change is related with microcracking, rose from ∌1.68 to ∌1.8. Porosity also increased (7.33–8.1%) from the beginning to the end of the experiment. Fluid/rock reactions were modeled with PHREEQC-2, and they are dominated by the dissolution of Mg-calcite. Mass balances show that ∌4% of the initial carbonate was consumed. The results suggest that mineral dissolution and microcracking may have acted in a synergistic way at the beginning of the acidic flooding. However, dissolution processes concentrated in pore throats can better explain the permeability enhancement observed over longer periods of time

    Suppl. material for JIFF 23524588-20230007 - Dietary application of <em>Hermetia illucens</em> larvae meal negatively affected the fillet quality and fatty acid metabolism of pearl gentian grouper

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    Black soldier fly (Hermetia illucens) (BSF) is an insect that can be fed with food waste, and its larval meal is now studied as a feed ingredient to reduce the use of fish meal. However, adding BSF into the feed of pearl gentian grouper (Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂) did not give good results. Higher levels of BSF substitution caused disorders of fatty acid metabolism, leads to fatty liver, and caused oxidative damage in the liver. Also, higher levels of BSF substitution reduced percentage of thick myofibers and significantly affected 40 of metabolites, including dodecanoic acid, D-lyxose, D-aspartic acid, and glutathione in the muscle, which did no positive effect on the improvement of fish meat. Therefore, BSF may require further processing, such as degreasing, in order to be better used. </p

    P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development

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    It has been shown that p53 has a critical role in the differentiation and functionality of various multipotent progenitor cells. P53 mutations can lead to genome instability and subsequent functional alterations and aberrant transformation of mesenchymal stem cells (MSCs). The significance of p53 in safeguarding our body from developing osteosarcoma (OS) is well recognized. During bone remodeling, p53 has a key role in negatively regulating key factors orchestrating the early stages of osteogenic differentiation of MSCs. Interestingly, changes in the p53 status can compromise bone homeostasis and affect the tumor microenvironment. This review aims to provide a unique opportunity to study the p53 function in MSCs and OS. In the context of loss of function of p53, we provide a model for two sources of OS: MSCs as progenitor cells of osteoblasts and bone tumor microenvironment components. Standing at the bone remodeling point of view, in this review we will first explain the determinant function of p53 in OS development. We will then summarize the role of p53 in monitoring MSC fidelity and in regulating MSC differentiation programs during osteogenesis. Finally, we will discuss the importance of loss of p53 function in tissue microenvironment. We expect that the information provided herein could lead to better understanding and treatment of OS

    Adsorption and Diffusion of Light Hydrocarbons in UiO-66(Zr): A Combination of Experimental and Modeling Tools

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    The concentration dependence of the self-diffusivity of short-chain linear alkanes in the narrow window type metal–organic framework (MOF) UiO-66­(Zr) has been studied by means of quasi-elastic neutron scattering (QENS) measurements combined with molecular dynamics (MD) simulations. These computations employ a force field to describe the host/guest interactions which was preliminarily validated on the adsorption data obtained for the system of interest via gravimetry and microcalorimetry measurements. The QENS-measured self-diffusivity profile presents a nonmonotonic tendency as the alkane loading increases, with the existence of a maximum that depends on the size of the alkane. The comparison with the simulated results obtained using either a flexible or a rigid framework highlights that the consideration of the flexibility is of prime importance when exploring the diffusion of ethane molecules in porous materials. The self-diffusivities subsequently calculated for propane and <i>n</i>-butane corroborate the results obtained for ethane, leading to a similar form for the plots of self-diffusion coefficient vs loading. The global microscopic diffusion mechanism is further shown to involve a combination of intracage motions and jump sequences between the tetrahedral and octahedral cages of the framework. The self-diffusion coefficients which decrease with increasing molecular size, and thus increasing confinement, are further compared to the values previously reported for MOFs with pore networks of different dimensions

    Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study

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    Importance: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. Objective: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. Data Sources: Genomewide association studies (GWAS) published up to January 15, 2015. Study Selection: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. Data Extraction and Synthesis: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. Main Outcomes and Measures: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. Results: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95% CI, 0.05-0.15]). Conclusions and Relevance: It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases

    Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function

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    Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways
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