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Cellulose-based superabsorbent was synthesized by bacterial cellulose (BC) grafting acrylic acid (AA) in the presence of N,N′-methylenebisacrylamide (NMBA) as a crosslinker and ammonium persulfate (APS) as an initiator. The influence of different factors on composite synthesis, including the weight ratio of the monomer to BC, initiator content, crosslinker content, AA neutralization degree, reaction temperature, and reaction time on the water absorbency of the composite, were systematically learned. Under the optimized conditions, the maximum water absorbency of the composite was 322 ± 23 g/g distilled water. However, the water absorbency was much less for the different salt solutions and the absorption capacity of the composite decreased as the concentration of the salt solutions increased. The pH value had a significant influence on water absorption performance, and with the increase of temperature, the water retention rate of the composite decreased. Additionally, the structure of this composite was characterized with nuclear magnetic resonance (NMR), Fourier transform infrared spectroscopy (FT-IR), scanning electron microscopy (SEM), and thermogravimetric analysis (TGA). The results of NMR and FT-IR provided evidence that the composite was synthesized by BC and AA, and the microstructure showed that it had good performance for water absorption. In addition, the composite possessed suitable thermal stability, and that it could be used in a few high-temperature environments. Overall, this composite is promising for application in water absorption. [ABSTRACT FROM AUTHOR]

Although the causal relationship between Alzheimer's disease (AD) and iron overload remains unclear, iron dyshomeostasis or improper transport mechanisms are speculated to lead to the accumulation of this neurotoxic metal in the hippocampal formation and other cerebral areas related to neurodegenerative diseases, resulting in the formation of reactive oxygen species (ROS) and, ultimately, cell death. In this study, exposure to high dietary iron (HDI) revealed no significant difference in the number of iron-positive cells and iron content in the cortex and hippocampal region between wild-type (WT) and APP/PS1 mice; however, compared with the control mice, the HDI-treated mice exhibited upregulated divalent metal transporter 1 (DMT1) and ferroportin (Fpn) expression, and downregulated transferrin receptor (TFR) expression. Importantly, we confirmed that there were significantly fewer NeuN-positive neurons in both APP/PS1 and WT mice given HDI, than in the respective controls. Moreover, this iron-induced neuron loss may involve increased ROS and oxidative mitochondria dysfunction, decreased DNA repair, and exacerbated apoptosis and autophagy. Although HDI administration might trigger protective antioxidant, anti-apoptosis, and autophagy signaling, especially in pathological conditions, these data clearly indicate that chronic iron exposure results in neuronal loss due to apoptosis, autophagy, and ferroptosis, hence increasing the risk for developing AD. [ABSTRACT FROM AUTHOR]