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Zeolite 4A was successfully prepared by hydrothermal synthesis using low-grade kaolin as a raw material. The properties of the synthesized zeolite 4A were characterized by means of X-ray diffraction (XRD), Fourier transform infrared (FTIR), 29Si magic-angle spinning (MAS)-nuclear magnetic resonance (NMR) and 27Al MAS-NMR, X-ray fluorescence (XRF), scanning electron microscopy (SEM)-energy-dispersive spectrometry (EDS), transmission electron microscopy (TEM), Brunauer–Emmett–Teller (BET), thermogravimetry (TG)-differential thermal analysis (DTA), and carbon dioxide adsorption analysis. The textural properties of the synthesized zeolite 4A was further studied by BET analysis technique. The thermal stability analysis showed that the heat resistance of the synthesized zeolite 4A is up to 940 °C. In addition, it is found that the Langmuir model has the best agreement with the adsorption equilibrium data for carbon dioxide by synthesized zeolite 4A and commercial zeolite 4A. Meanwhile, the carbon dioxide adsorption analysis confirmed that the maximum equilibrium adsorption amount of carbon dioxide on synthesized zeolite 4A is 59.3820 mL/g, which is higher than the 55.4303 mL/g of the commercial zeolite 4A.

Background: Increased circulating endothelial microparticles (EMPs) have been shown to associate with endothelial dysfunction. We explored the effect of iron on EMP generation by human umbilical vein endothelial cells (HUVECs) and the potential protective effect of carvedilol. Methods: FeCl₃ was added to HUVEC culture. Iron entry into cells was monitored using fluorescent microscopic imaging, while the quantity of EMPs that was released was determined by flow cytometry. The apoptosis of HUVECs was assessed by annexin V/propidium iodide assay and caspase-3 expression. Membrane bleb formation was visualized using electron microscopy. Intracellular production of reactive oxygen species (ROS) was also monitored. The effects of beta-blockers, carvedilol and propranolol on these processes were determined by co-incubation in a dose-dependent manner. Iron entry into HUVECs was not blocked by either beta-blocker. Iron induced the generation of EMPs, the formation of membrane blebs, the apoptosis of HUVECs and the production of ROS, each in a dose-dependent manner. Carvedilol, but not propranolol, ameliorated all of these processes. Results: Our result indicates that iron induces EMP generation and apoptosis of endothelial cells in association with increased oxidative stress. Conclusion: The protective effects of carvedilol, via its antioxidant effect, may have therapeutic potential in patients with iron overload.

Dielectric composites based on ferroelectric ceramics nanofibers are attracting increasing attention in capacitor application. In this work, the sol–gel method and electrospinning technology are utilized to prepare one-dimensional Na0.5Bi0.5TiO3 (NBT) nanofibers, and the influence of electrospinning process parameters such as spinning voltage, liquid supply rate, and collector speed on the morphology and structure of nanofibers are systematically explored. The final optimized parameters include the applied voltage of 20 kV, the solution flow rate of 1 mL/h, and the collector’s rotation speed of 1500 rpm. The optimized NBT nanofibers are introduced into the PVDF polymer matrix for energy storage application. Owing to the enhanced interfacial polarization between PVDF matrix and NBT nanofibers with a high aspect ratio, the NBT–PVDF nanocomposites achieve a high discharge energy density of 14.59 J cm−3 and an energy efficiency of 53.69% at 490 kV mm−1, which are higher than those of pure PVDF, i.e., 10.26 J cm−3 and 48.17% at 420 kV mm−1, respectively. The results demonstrate that the strategy of synthesizing NBT nanofibers using the electrospinning method is of great potential for high-performance dielectric capacitor application.

Purpose This review aimed to provide an overview of current research into the risk factors for Graves' ophthalmopathy (GO). Methods To find information about the risk factors for GO, the research database PubMed was searched and relevant articles were obtained to extract information about risk factors. Results Smoking has been widely accepted as an important risk factor and cigarette smoking cessation has been shown to improve the outcome and decrease the onset of GO. Radioactive iodine on the thyroid may induce hyperthyroidism and increase the occurrence of GO. Selenium deficiency is a risk factor for GO and the supplementation of selenium has been an adjuvant therapy. Decreasing stressful life events (SLE) may help improve GO. Imbalance in intestinal flora is essential to GO, with Yersinia enterocolitica and Escherichia coli both increased in the digestive tract of the individual with GO. In addition, controlling serum cholesterol may help improve GO since adipogenesis is an important pathological change in its pathogenesis. Considering the correlation between Graves' disease and GO, maintaining normal thyroid function hormone level is the first-line therapeutic strategy to prevent progression of GO. An increase in antibodies such as TSHR and IGF-1R is the main predictor of GO. Besides, gender and gene polymorphism are also risk factors towards GO. Conclusions Risk factors for GO arise from five sources: physical and chemical environment, social-psychological environment, biological environment, the human organism, and genetic codes. Risk factors within these categories may interact with each other and their mechanisms in promoting the development of GO are complex. Research into risk factors for GO may promote emerging fields related to GO such as control of autoantibodies and intestinal microbiota.

Background and aims The activation of orbital fibroblasts, the prime targets in thyroid eye disease, is central to its underlying pathogenesis. We aimed to investigate the mechanism of thyroid eye disease orbital fibroblast activation from the perspective of non-coding RNA regulation. Methods Immunofluorescence (IF) staining was applied to evaluate the fibrotic changes in target cells. Cell proliferation were evaluated by EDU and colony formation assays. Collagen I concentration was determined by ELISA assay. Human microarray analysis was performed on three thyroid eye disease and 3 healthy control orbital tissue samples. Results Bioinformatics analysis showed that cell adhesion signaling factors were differentially expressed in thyroid eye disease tissues, including I-CAM-1, I-CAM-4, V-CAM, and CD44, which were all upregulated in diseased orbital tissues. LncRNA LPAL2 level was also upregulated in orbital tissues and positively correlated with I-CAM-1 and I-CAM-4 expression. Stimulation of the thyroid eye disease orbital fibroblasts by TGF-β1 significantly increased the expression of I-CAM-1, I-CAM-4, and LPAL2. Knockdown of LPAL2 in orbital fibroblasts inhibited TGF-β1-induced increases in cell adhesion factor levels and orbital fibroblast activation. Microarray profiling was performed on thyroid eye disease and normal orbital tissues to identify differentially expressed miRNAs and miR-1287-5p was remarkably reduced within diseased orbital samples. miR-1287-5p was directly bound to EGFR 3’UTR and LPAL2 and LPAL2 modulated EGFR/AKT signaling through targeting miR-1287-5p. Conclusions The LPAL2/miR-1287-5p axis modulated TGF-β1-induced increases in cell adhesion factor levels and thyroid eye disease orbital fibroblast activation through EGFR/AKT signaling.